<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">LaPallo, Brandon K.</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Spinal transection alters external urethral sphincter activity during spontaneous voiding in freely-moving rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurotrauma</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">May</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28467736</style></url></web-urls></urls><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The rat is a commonly used model for the study of lower urinary tract function before and after spinal cord injury. We have previously reported that in unanesthetized, freely-moving rats, although phasic external urethral sphincter (EUS) activity (bursting) is most common during micturition, productive voiding can occur in the absence of bursting, which differs from results seen in anesthetized or unanesthetized restrained animals. The purpose of the present study was to characterize EUS behavior in unanesthetized, freely-moving rats before and after mid-thoracic (T8) or thoraco-lumbar (T13-L1) spinal transection to determine how EUS behavior after spinal cord injury differs from that seen in anesthetized or unanesthetized restrained rats. Several abnormalities became evident that were comparable after transection at either level including: repetitive non-voiding EUS contractions; increased prevalence, intensity and duration of EUS bursting; decreased rate of urine evacuation during bursting; increased void size and decreased number of daily voids; shorter inter-burst silent period and increased frequency of bursting; and loss of the direct linear relationships that are evident in intact animals between void size and bursting silent period. These data suggest that transection-induced delayed initiation of EUS bursting allows co-contraction of the bladder and the EUS that prevents or limits urine evacuation, resulting in a detrusor-sphincter dyssynergia-like phenomenon. In addition, the higher-than-normal frequency at which EUS bursting occurs after transection is associated with shorter silent periods during which urine typically flows, which interferes with voiding by slowing the rate of urine evacuation. That results were comparable after either transection suggests that the central pattern generator responsible for EUS bursting is located caudal to the L1 spinal segment.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Wang, Yu</style></author><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Chen, Lu</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Ablation of the inferior olive prevents H-reflex down-conditioning in rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Mar</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26792888</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">115</style></volume><pages><style face="normal" font="default" size="100%">1630–1636</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">We evaluated the role of the inferior olive (IO) in acquisition of the spinal cord plasticity that underlies H-reflex down-conditioning, a simple motor skill. The IO was chemically ablated before a 50-day exposure to an operant conditioning protocol that rewarded a smaller soleus H-reflex. In normal rats, down-conditioning succeeds (i.e., H-reflex size decreases at least 20%) in 80% of animals. Down-conditioning failed in every IO-ablated rat (P&lt; 0.001 vs. normal rats). IO ablation itself had no long-term effect on H-reflex size. These results indicate that the IO is essential for acquisition of a down-conditioned H-reflex. With previous data, they support the hypothesis that IO and cortical inputs to cerebellum enable the cerebellum to guide sensorimotor cortex plasticity that produces and maintains the spinal cord plasticity that underlies the down-conditioned H-reflex. They help to further define H-reflex conditioning as a model for understanding motor learning and as a new approach to enhancing functional recovery after trauma or disease.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">LaPallo, Brandon K.</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Contribution of the external urethral sphincter to urinary void size in unanesthetized unrestrained rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Neurourology and urodynamics</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Aug</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25995074</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">35</style></volume><pages><style face="normal" font="default" size="100%">696–702</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">In anesthetized rats, voiding is typically associated with phasic activation (bursting) of the external urethral sphincter (EUS). During spontaneous voiding in unanesthetized, unrestrained rats, EUS bursting is the most common form of EUS activity exhibited, but it is not necessary for productive voiding to occur. The aim of the present study was to determine which aspects of EUS activity contributed to void size during bursting and non-bursting voiding in conscious, freely moving rats.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Wang, Yu</style></author><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Chen, Lu</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The inferior olive is essential for long-term maintenance of a simple motor skill.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Oct</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27535367</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">116</style></volume><pages><style face="normal" font="default" size="100%">1946–1955</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The inferior olive (IO) is essential for operant down-conditioning of the rat soleus H-reflex, a simple motor skill. To evaluate the role of the IO in long-term maintenance of this skill, the H-reflex was down-conditioned over 50 days, the IO was chemically ablated, and down-conditioning continued for up to 102 more days. H-reflex size just before IO ablation averaged 62(±2 SE)% of its initial value (P &lt; 0.001 vs. initial). After IO ablation, H-reflex size rose to 75-80% over ?10 days, remained there for ?30 days, rose over 10 days to above its initial value, and averaged 140(±14)% for the final 10 days of study (P &lt; 0.01 vs. initial). This two-stage loss of down-conditioning maintenance correlated with IO neuronal loss (r = 0.75, P &lt; 0.01) and was similar to the loss of down-conditioning that follows ablation of the cerebellar output nuclei dentate and interpositus. In control (i.e., unconditioned) rats, IO ablation has no long-term effect on H-reflex size. These results indicate that the IO is essential for long-term maintenance of a down-conditioned H-reflex. With previous data, they support the hypothesis that IO and cortical inputs to cerebellum combine to produce cerebellar plasticity that produces sensorimotor cortex plasticity that produces spinal cord plasticity that produces the smaller H-reflex. H-reflex down-conditioning appears to depend on a hierarchy of plasticity that may be guided by the IO and begin in the cerebellum. Similar hierarchies may underlie other motor learning.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Chadwick B. Boulay</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Electrocorticographic activity over sensorimotor cortex and motor function in awake behaving rats.</style></title><secondary-title><style face="normal" font="default" size="100%">J Neurophysiol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Neurophysiol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">brain-computer interface</style></keyword><keyword><style  face="normal" font="default" size="100%">cortex</style></keyword><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">Motor control</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">04/2015</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25632076</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">113</style></volume><pages><style face="normal" font="default" size="100%">2232-41</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Sensorimotor cortex exerts both short-term and long-term control over the spinal reflex pathways that serve motor behaviors. Better understanding of this control could offer new possibilities for restoring function after central nervous system trauma or disease. We examined the impact of ongoing sensorimotor cortex (SMC) activity on the largely monosynaptic pathway of the H-reflex, the electrical analog of the spinal stretch reflex. In 41 awake adult rats, we measured soleus electromyographic (EMG) activity, the soleus H-reflex, and electrocorticographic activity over the contralateral SMC while rats were producing steady-state soleus EMG activity. Principal component analysis of electrocorticographic frequency spectra before H-reflex elicitation consistently revealed three frequency bands: μβ (5-30 Hz), low γ (γ1; 40-85 Hz), and high γ (γ2; 100-200 Hz). Ongoing (i.e., background) soleus EMG amplitude correlated negatively with μβ power and positively with γ1 power. In contrast, H-reflex size correlated positively with μβ power and negatively with γ1 power, but only when background soleus EMG amplitude was included in the linear model. These results support the hypothesis that increased SMC activation (indicated by decrease in μβ power and/or increase in γ1 power) simultaneously potentiates the H-reflex by exciting spinal motoneurons and suppresses it by decreasing the efficacy of the afferent input. They may help guide the development of new rehabilitation methods and of brain-computer interfaces that use SMC activity as a substitute for lost or impaired motor outputs.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">7</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Ran, Bo</style></author><author><style face="normal" font="default" size="100%">Zhang, Guo-You</style></author><author><style face="normal" font="default" size="100%">Shen, Feng</style></author><author><style face="normal" font="default" size="100%">Chen, Jia-Yu</style></author><author><style face="normal" font="default" size="100%">Wu, Ji-Bin</style></author><author><style face="normal" font="default" size="100%">Zhao, Feng-Chao</style></author><author><style face="normal" font="default" size="100%">Guo, Kai-Jin</style></author><author><style face="normal" font="default" size="100%">Qi, Dun-Yi</style></author><author><style face="normal" font="default" size="100%">Zhou, Bing</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Zhang, Xin-Zhu</style></author><author><style face="normal" font="default" size="100%">Qiao, Yue-Hua</style></author><author><style face="normal" font="default" size="100%">Li, Ming</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Retraction Note: Comparison of the sagittal profiles among thoracic idiopathic scoliosis patients with different Cobb angles and growth potentials.</style></title><secondary-title><style face="normal" font="default" size="100%">J Orthop Surg Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Orthop Surg Res</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">03/2015</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25886636</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">10</style></volume><pages><style face="normal" font="default" size="100%">44</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">1</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Wang, Ru-Feng</style></author><author><style face="normal" font="default" size="100%">Liu, Bin</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">An update on oligosaccharides and their esters from traditional chinese medicines: chemical structures and biological activities.</style></title><secondary-title><style face="normal" font="default" size="100%">Evid Based Complement Alternat Med</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Evid Based Complement Alternat Med</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">03/2015</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25861364</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">2015</style></volume><pages><style face="normal" font="default" size="100%">512675</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;A great number of naturally occurring oligosaccharides and oligosaccharide esters have been isolated from traditional Chinese medicinal plants, which are used widely in Asia and show prominent curative effects in the prevention and treatment of kinds of diseases. Numerous in vitro and in vivo experiments have revealed that oligosaccharides and their esters exhibited various activities, including antioxidant, antidepressant, cytotoxic, antineoplastic, anti-inflammatory, neuroprotective, cerebral protective, antidiabetic, plant growth-regulatory, and immunopotentiating activities. This review summarizes the investigations on the distribution, chemical structures, and bioactivities of natural oligosaccharides and their esters from traditional Chinese medicines between 2003 and 2013.&lt;/p&gt;</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Lv, You</style></author><author><style face="normal" font="default" size="100%">Xia, Jie-yun</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Zhao, Hui</style></author><author><style face="normal" font="default" size="100%">Yan, Hai-cui</style></author><author><style face="normal" font="default" size="100%">Yang, Han-shi</style></author><author><style face="normal" font="default" size="100%">Li, Qiang</style></author><author><style face="normal" font="default" size="100%">Fan, Yu-xin</style></author><author><style face="normal" font="default" size="100%">Guo, Kai-Jin</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Effects of pamidronate disodium on the loss of osteoarthritic subchondral bone and the expression of cartilaginous and subchondral osteoprotegerin and RANKL in rabbits.</style></title><secondary-title><style face="normal" font="default" size="100%">BMC Musculoskelet Disord</style></secondary-title><alt-title><style face="normal" font="default" size="100%">BMC Musculoskelet Disord</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">cartilage</style></keyword><keyword><style  face="normal" font="default" size="100%">osteoarthritis</style></keyword><keyword><style  face="normal" font="default" size="100%">osteoprotegerin (OPG)</style></keyword><keyword><style  face="normal" font="default" size="100%">pamidronate disodium</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptor activator of nuclear factor-κ B ligand (RANKL)</style></keyword><keyword><style  face="normal" font="default" size="100%">subchondral bone</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">11/2014</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25377946</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">15</style></volume><pages><style face="normal" font="default" size="100%">370</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Osteoarthritis (OA) is a major health problem in the increasingly elderly population. Therefore, it is crucial to prevent and treat OA at an early stage. The present study investigated whether pamidronate disodium (PAM), a bone-loss inhibitor, can significantly prevent or reverse the progression of early anterior cruciate ligament transection (ACLT)-induced OA. Whether therapeutic intervention is associated with regulation of the expression of osteoprotegerin (OPG), receptor activator of nuclear factor-κB ligand (RANKL), metalloproteinase-9 (MMP-9) or Toll-like receptor-4 (TLR-4) in cartilage and/or subchondral bone was also investigated.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;60 New Zealand rabbits were randomized into four groups: Sham-operated (n = 20); ACLT (n = 20); short-term treatment with PAM (PAM-S, n = 10) and long-term treatment with PAM (PAM-L, n = 10). For cartilage and subchondral bone testing, rabbits from Sham and ACLT groups were harvested at 2, 4, 6, and 14 weeks. Rabbits were given PAM from the 4th week after ACLT operation in PAM-S and PAM-L group, and were harvested at 6 and 14 weeks, respectively. Trabecular characteristics and cartilage changes were detected using Micro-CT, safranin O and rapid green staining, respectively. Immunohistochemical staining for OPG and RANKL were also performed. OPG, RANKL, MMP-9 and TLR-4 expression was evaluated by western blot analysis.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Micro-CT and histology analyses indicated that PAM treatment for 2 or 10 weeks could completely prevent or reverse osteoarthritic subchondral bone loss and cartilage surface erosion. Immunohistochemistry and western blot analysis indicated that expression of OPG and RANKL increased, although RANKL expression increased more significantly than that of OPG. Therefore the ratio of OPG to RANKL was lower in the ACLT group. However, the ratio of OPG to RANKL in the PAM group was significantly higher than that in the ACLT group. Additionally, expression of MMP-9 and TLR-4 were upregulated in the ACLT group and downregulated in the PAM treated groups.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;PAM can significantly inhibit and even reverse early osteoarthritic subchondral bone loss, thus alleviating the process of cartilaginous degeneration. The mechanisms involved may be associated with the upregulation of OPG expression, and downregulation of RANKL, MMP-9 and TLR-4 expression.&lt;/p&gt;</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Ran, Bo</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Zhang, Guo-You</style></author><author><style face="normal" font="default" size="100%">Shen, Feng</style></author><author><style face="normal" font="default" size="100%">Chen, Jia-Yu</style></author><author><style face="normal" font="default" size="100%">Wu, Ji-Bin</style></author><author><style face="normal" font="default" size="100%">Zhao, Feng-Chao</style></author><author><style face="normal" font="default" size="100%">Qiao, Dun-Yi</style></author><author><style face="normal" font="default" size="100%">Zhou, Bing</style></author><author><style face="normal" font="default" size="100%">Zhang, Xin-Zhu</style></author><author><style face="normal" font="default" size="100%">Qiao, Yue-Hua</style></author><author><style face="normal" font="default" size="100%">Guan, Jun-Hui</style></author><author><style face="normal" font="default" size="100%">Guo, Kai-Jin</style></author><author><style face="normal" font="default" size="100%">Li, Ming</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Erratum: comparison of the sagittal profiles among thoracic idiopathic scoliosis patients with different Cobb angles and growth potentials.</style></title><secondary-title><style face="normal" font="default" size="100%">J Orthop Surg Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Orthop Surg Res</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">10/2014</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25927908</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">9</style></volume><pages><style face="normal" font="default" size="100%">82</style></pages><language><style face="normal" font="default" size="100%">eng</style></language></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Liu, Rongliang</style></author><author><style face="normal" font="default" size="100%">Wang, Yu</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Locomotor impact of beneficial or nonbeneficial H-reflex conditioning after spinal cord injury.</style></title><secondary-title><style face="normal" font="default" size="100%">J Neurophysiol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Neurophysiol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Conditioning, Operant</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">Learning</style></keyword><keyword><style  face="normal" font="default" size="100%">Locomotion</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats, Sprague-Dawley</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord Injuries</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">03/2014</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24371288</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">111</style></volume><pages><style face="normal" font="default" size="100%">1249-58</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">When new motor learning changes neurons and synapses in the spinal cord, it may affect previously learned behaviors that depend on the same spinal neurons and synapses. To explore these effects, we used operant conditioning to strengthen or weaken the right soleus H-reflex pathway in rats in which a right spinal cord contusion had impaired locomotion. When up-conditioning increased the H-reflex, locomotion improved. Steps became longer, and step-cycle asymmetry (i.e., limping) disappeared. In contrast, when down-conditioning decreased the H-reflex, locomotion did not worsen. Steps did not become shorter, and asymmetry did not increase. Electromyographic and kinematic analyses explained how H-reflex increase improved locomotion and why H-reflex decrease did not further impair it. Although the impact of up-conditioning or down-conditioning on the H-reflex pathway was still present during locomotion, only up-conditioning affected the soleus locomotor burst. Additionally, compensatory plasticity apparently prevented the weaker H-reflex pathway caused by down-conditioning from weakening the locomotor burst and further impairing locomotion. The results support the hypothesis that the state of the spinal cord is a &quot;negotiated equilibrium&quot; that serves all the behaviors that depend on it. When new learning changes the spinal cord, old behaviors undergo concurrent relearning that preserves or improves their key features. Thus, if an old behavior has been impaired by trauma or disease, spinal reflex conditioning, by changing a specific pathway and triggering a new negotiation, may enable recovery beyond that achieved simply by practicing the old behavior. Spinal reflex conditioning protocols might complement other neurorehabilitation methods and enhance recovery.</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">LaPallo, Brandon K</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Long-term recording of external urethral sphincter EMG activity in unanesthetized, unrestrained rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Am J Physiol Renal Physiol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Am. J. Physiol. Renal Physiol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Electrodes, Implanted</style></keyword><keyword><style  face="normal" font="default" size="100%">Electromyography</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Pubic Bone</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats, Sprague-Dawley</style></keyword><keyword><style  face="normal" font="default" size="100%">Urethra</style></keyword><keyword><style  face="normal" font="default" size="100%">Urination</style></keyword><keyword><style  face="normal" font="default" size="100%">Urodynamics</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">08/2014</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24990895</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">307</style></volume><pages><style face="normal" font="default" size="100%">F485-97</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The external urethral sphincter muscle (EUS) plays an important role in urinary function and often contributes to urinary dysfunction. EUS study would benefit from methodology for longitudinal recording of electromyographic activity (EMG) in unanesthetized animals, but this muscle is a poor substrate for chronic intramuscular electrodes, and thus the required methodology has not been available. We describe a method for long-term recording of EUS EMG by implantation of fine wires adjacent to the EUS that are secured to the pubic bone. Wires pass subcutaneously to a skull-mounted plug and connect to the recording apparatus by a flexible cable attached to a commutator. A force transducer-mounted cup under a metabolic cage collected urine, allowing recording of EUS EMG and voided urine weight without anesthesia or restraint. Implant durability permitted EUS EMG recording during repeated (up to 3 times weekly) 24-h sessions for more than 8 wk. EMG and voiding properties were stable over weeks 2-8. The degree of EUS phasic activity (bursting) during voiding was highly variable, with an average of 25% of voids not exhibiting bursting. Electrode implantation adjacent to the EUS yielded stable EMG recordings over extended periods and eliminated the confounding effects of anesthesia, physical restraint, and the potential for dislodgment of the chronically implanted intramuscular electrodes. These results show that micturition in unanesthetized, unrestrained rats is usually, but not always, associated with EUS bursting. This methodology is applicable to studying EUS behavior during progression of gradually evolving disease and injury models and in response to therapeutic interventions.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Wang, Yu</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Persistent beneficial impact of H-reflex conditioning in spinal cord-injured rats.</style></title><secondary-title><style face="normal" font="default" size="100%">J Neurophysiol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Neurophysiol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">H-reflex conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">Learning</style></keyword><keyword><style  face="normal" font="default" size="100%">Locomotion</style></keyword><keyword><style  face="normal" font="default" size="100%">Memory</style></keyword><keyword><style  face="normal" font="default" size="100%">Motor control</style></keyword><keyword><style  face="normal" font="default" size="100%">Rehabilitation</style></keyword><keyword><style  face="normal" font="default" size="100%">spinal cord injury</style></keyword><keyword><style  face="normal" font="default" size="100%">spinal cord plasticity</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">11/2014</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25143542</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">112</style></volume><pages><style face="normal" font="default" size="100%">2374-81</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Operant conditioning of a spinal cord reflex can improve locomotion in rats and humans with incomplete spinal cord injury. This study examined the persistence of its beneficial effects. In rats in which a right lateral column contusion injury had produced asymmetric locomotion, up-conditioning of the right soleus H-reflex eliminated the asymmetry while down-conditioning had no effect. After the 50-day conditioning period ended, the H-reflex was monitored for 100 [±9 (SD)] (range 79-108) more days and locomotion was then reevaluated. After conditioning ended in up-conditioned rats, the H-reflex continued to increase, and locomotion continued to improve. In down-conditioned rats, the H-reflex decrease gradually disappeared after conditioning ended, and locomotion at the end of data collection remained as impaired as it had been before and immediately after down-conditioning. The persistence (and further progression) of H-reflex increase but not H-reflex decrease in these spinal cord-injured rats is consistent with the fact that up-conditioning improved their locomotion while down-conditioning did not. That is, even after up-conditioning ended, the up-conditioned H-reflex pathway remained adaptive because it improved locomotion. The persistence and further enhancement of the locomotor improvement indicates that spinal reflex conditioning protocols might supplement current therapies and enhance neurorehabilitation. They may be especially useful when significant spinal cord regeneration becomes possible and precise methods for retraining the regenerated spinal cord are needed.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">10</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Thompson, Aiko K.</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Soleus H-reflex operant conditioning changes the H-reflex recruitment curve.</style></title><secondary-title><style face="normal" font="default" size="100%">Muscle &amp; nerve</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">motor learning</style></keyword><keyword><style  face="normal" font="default" size="100%">plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">Rehabilitation</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">04/2013</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/23281107</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">47</style></volume><pages><style face="normal" font="default" size="100%">539–544</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">INTRODUCTION:
Operant conditioning can gradually change the human soleus H-reflex. The protocol conditions the reflex near M-wave threshold. In this study we examine its impact on the reflexes at other stimulus strengths.
METHODS:
H-reflex recruitment curves were obtained before and after a 24-session exposure to an up-conditioning (HRup) or a down-conditioning (HRdown) protocol and were compared.
RESULTS:
In both HRup and HRdown subjects, conditioning affected the entire H-reflex recruitment curve. In 5 of 6 HRup and 3 of 6 HRdown subjects, conditioning elevated (HRup) or depressed (HRdown), respectively, the entire curve. In the other HRup subject or the other 3 HRdown subjects, the curve was shifted to the left or to the right, respectively.
CONCLUSIONS:
H-reflex conditioning does not simply change the H-reflex to a stimulus of particular strength; it also changes the H-reflexes to stimuli of different strengths. Thus, it is likely to affect many actions in which this pathway participates.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Wang, Yu</style></author><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cortical stimulation causes long-term changes in H-reflexes and spinal motoneuron GABA receptors.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">11/2012</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22933718</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">108</style></volume><pages><style face="normal" font="default" size="100%">2668–2678</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The cortex gradually modifies the spinal cord during development, throughout later life, and in response to trauma or disease. The mechanisms of this essential function are not well understood. In this study, weak electrical stimulation of rat sensorimotor cortex increased the soleus H-reflex, increased the numbers and sizes of GABAergic spinal interneurons and GABAergic terminals on soleus motoneurons, and decreased GABA(A) and GABA(B) receptor labeling in these motoneurons. Several months after the stimulation ended the interneuron and terminal increases had disappeared, but the H-reflex increase and the receptor decreases remained. The changes in GABAergic terminals and GABA(B) receptors accurately predicted the changes in H-reflex size. The results reveal a new long-term dimension to cortical-spinal interactions and raise new therapeutic possibilities.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Wang, Yu</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Operant conditioning of rat soleus H-reflex oppositely affects another H-reflex and changes locomotor kinematics.</style></title><secondary-title><style face="normal" font="default" size="100%">The Journal of neuroscience : the official journal of the Society for Neuroscience</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Sprague-Dawley</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">08/2011</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21813696</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">31</style></volume><pages><style face="normal" font="default" size="100%">11370–11375</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">H-reflex conditioning is a model for studying the plasticity associated with a new motor skill. We are exploring its effects on other reflexes and on locomotion. Rats were implanted with EMG electrodes in both solei (SOL(R) and SOL(L)) and right quadriceps (QD(R)), and stimulating cuffs on both posterior tibial (PT) nerves and right posterior femoral nerve. When SOL(R) EMG remained in a defined range, PT(R) stimulation just above M-response threshold elicited the SOL(R) H-reflex. Analogous procedures elicited the QD(R) and SOL(L) H-reflexes. After a control period, each rat was exposed for 50 d to a protocol that rewarded SOL(R) H-reflexes that were above (HRup rats) or below (HRdown rats) a criterion. HRup conditioning increased the SOL(R) H-reflex to 214 ± 37% (mean ± SEM) of control (p = 0.02) and decreased the QD(R) H-reflex to 71 ± 26% (p = 0.06). HRdown conditioning decreased the SOL(R) H-reflex to 69 ± 2% (p &lt; 0.001) and increased the QD(R) H-reflex to 121 ± 7% (p = 0.02). These changes remained during locomotion. The SOL(L) H-reflex did not change. During the stance phase of locomotion, ankle plantarflexion increased in HRup rats and decreased in HRdown rats, hip extension did the opposite, and hip height did not change. The plasticity that changes the QD(R) H-reflex and locomotor kinematics may be inevitable (i.e., reactive) due to the ubiquity of activity-dependent CNS plasticity, and/or necessary (i.e., compensatory) to preserve other behaviors (e.g., locomotion) that would otherwise be disturbed by the change in the SOL(R) H-reflex pathway. The changes in joint angles, coupled with the preservation of hip height, suggest that compensatory plasticity did occur.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Sun, Chenyou</style></author><author><style face="normal" font="default" size="100%">Wang, Yu</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">WITHDRAWN: H-reflex up-conditioning after sciatic nerve transection and regeneration may increase VGLUT-1 terminals and GluR2/3 immunoreactivity in spinal motoneurons.</style></title><secondary-title><style face="normal" font="default" size="100%">Neuroscience letters</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">12/2011</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22198372</style></url></web-urls></urls><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at http://www.elsevier.com/locate/withdrawalpolicy.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Tennissen, Ann M.</style></author><author><style face="normal" font="default" size="100%">Liebschutz, Jennifer E.</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">External urethral sphincter motoneuron properties in adult female rats studied in vitro.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Urethra</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">09/2010</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20573976</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">104</style></volume><pages><style face="normal" font="default" size="100%">1286–1300</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The external urethral sphincter (EUS) muscle plays a crucial role in lower urinary tract function: its activation helps maintain continence, whereas its relaxation contributes to micturition. To determine how the intrinsic properties of its motoneurons contribute to its physiological function, we have obtained intracellular current-clamp recordings from 49 EUS motoneurons in acutely isolated spinal cord slices from adult female rats. In all, 45% of EUS motoneurons fired spontaneously and steadily (average rate = 12-27 pulses/s). EUS motoneurons were highly excitable, having lower rheobase, higher input resistance, and smaller threshold depolarization than those of rat hindlimb motoneurons recorded in vitro. Correlations between these properties and afterhyperpolarization half-decay time are consistent with EUS motoneurons having characteristics of both fast and slow motor unit types. EUS motoneurons with a slow-like spectrum of properties exhibited spontaneous firing more often than those with fast-like characteristics. During triangular current ramp-induced repetitive firing, recruitment typically occurred at lower current levels than those at derecruitment, although the opposite pattern occurred in 10% of EUS motoneurons. This percentage was likely underestimated due to firing rate adaptation. These findings are consistent with the presence of a basal level of persistent inward current (PIC) in at least some EUS motoneurons. The low EUS motoneuron current and voltage thresholds make them readily recruitable, rendering them well suited to their physiological role in continence. The expression of firing behaviors consistent with PIC activation in this highly reduced preparation raises the possibility that in the intact animal, PICs contribute to urinary function not only through neuromodulator-dependent but also through neuromodulator-independent mechanisms.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Wang, Yu</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Sun, Chenyou</style></author><author><style face="normal" font="default" size="100%">English, Arthur W.</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">H-reflex up-conditioning encourages recovery of EMG activity and H-reflexes after sciatic nerve transection and repair in rats.</style></title><secondary-title><style face="normal" font="default" size="100%">The Journal of neuroscience : the official journal of the Society for Neuroscience</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">peripheral nerve</style></keyword><keyword><style  face="normal" font="default" size="100%">plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">regeneration</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">12/2010</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21123559</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">30</style></volume><pages><style face="normal" font="default" size="100%">16128–16136</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Operant conditioning of the spinal stretch reflex or its electrical analog, the H-reflex, produces spinal cord plasticity and can thereby affect motoneuron responses to primary afferent input. To explore whether this conditioning can affect the functional outcome after peripheral nerve injury, we assessed the effect of up-conditioning soleus (SOL) H-reflex on SOL and tibialis anterior (TA) function after sciatic nerve transection and repair. Sprague Dawley rats were implanted with EMG electrodes in SOL and TA and stimulating cuffs on the posterior tibial nerve. After control data collection, the sciatic nerve was transected and repaired and the rat was exposed for 120 d to continued control data collection (TC rats) or SOL H-reflex up-conditioning (TU rats). At the end of data collection, motoneurons that had reinnervated SOL and TA were labeled retrogradely. Putative primary afferent terminals [i.e., terminals containing vesicular glutamate transporter-1 (VGLUT1)] on SOL motoneurons were studied immunohistochemically. SOL (and probably TA) background EMG activity recovered faster in TU rats than in TC rats, and the final recovered SOL H-reflex was significantly larger in TU than in TC rats. TU and TC rats had significantly fewer labeled motoneurons and higher proportions of double-labeled motoneurons than untransected rats. VGLUT1 terminals were significantly more numerous on SOL motoneurons of TU than TC rats. Combined with the larger H-reflexes in TU rats, this anatomical finding supports the hypothesis that SOL H-reflex up-conditioning strengthened primary afferent reinnervation of SOL motoneurons. These results suggest that H-reflex up-conditioning may improve functional recovery after nerve injury and repair.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Wang, Yu</style></author><author><style face="normal" font="default" size="100%">Thompson, Aiko</style></author><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Segal, Richard L.</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Reflex conditioning: a new strategy for improving motor function after spinal cord injury.</style></title><secondary-title><style face="normal" font="default" size="100%">Annals of the New York Academy of Sciences</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">learning and memory</style></keyword><keyword><style  face="normal" font="default" size="100%">Locomotion</style></keyword><keyword><style  face="normal" font="default" size="100%">plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">reflex conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">Rehabilitation</style></keyword><keyword><style  face="normal" font="default" size="100%">spinal cord injury</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">06/2010</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20590534</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">1198 Suppl 1</style></volume><pages><style face="normal" font="default" size="100%">E12–E21</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Spinal reflex conditioning changes reflex size, induces spinal cord plasticity, and modifies locomotion. Appropriate reflex conditioning can improve walking in rats after spinal cord injury (SCI). Reflex conditioning offers a new therapeutic strategy for restoring function in people with SCI. This approach can address the specific deficits of individuals with SCI by targeting specific reflex pathways for increased or decreased responsiveness. In addition, once clinically significant regeneration can be achieved, reflex conditioning could provide a means of reeducating the newly (and probably imperfectly) reconnected spinal cord.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Thompson, Aiko K.</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Acquisition of a simple motor skill: task-dependent adaptation plus long-term change in the human soleus H-reflex.</style></title><secondary-title><style face="normal" font="default" size="100%">The Journal of neuroscience : the official journal of the Society for Neuroscience</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">motor learning</style></keyword><keyword><style  face="normal" font="default" size="100%">motor skill</style></keyword><keyword><style  face="normal" font="default" size="100%">operant conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2009</style></year><pub-dates><date><style  face="normal" font="default" size="100%">05/2009</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/19420246</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">29</style></volume><pages><style face="normal" font="default" size="100%">5784–5792</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Activity-dependent plasticity occurs throughout the CNS. However, investigations of skill acquisition usually focus on cortex. To expand the focus, we analyzed in humans the development of operantly conditioned H-reflex change, a simple motor skill that develops gradually and involves plasticity in both the brain and the spinal cord. Each person completed 6 baseline and 24 conditioning sessions over 10 weeks. In each conditioning session, the soleus H-reflex was measured while the subject was or was not asked to increase (HRup subjects) or decrease (HRdown subjects) it. When the subject was asked to change H-reflex size, immediate visual feedback indicated whether a size criterion had been satisfied. Over the 24 conditioning sessions, H-reflex size gradually increased in six of eight HRup subjects and decreased in eight of nine HRdown subjects, resulting in final sizes of 140 +/- 12 and 69 +/- 6% of baseline size, respectively. The final H-reflex change was the sum of within-session (i.e., task-dependent) adaptation and across-session (i.e., long-term) change. Task-dependent adaptation appeared within four to six sessions and persisted thereafter, averaging +13% in HRup subjects and -15% in HRdown subjects. In contrast, long-term change began after 10 sessions and increased gradually thereafter, reaching +27% in HRup subjects and -16% in HRdown subjects. Thus, the acquisition of H-reflex conditioning consists of two phenomena, task-dependent adaptation and long-term change, that together constitute the new motor skill. In combination with previous data, this new finding further elucidates the interaction of plasticity in brain and spinal cord that underlies the acquisition and maintenance of motor skills.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Cheng, Jin</style></author><author><style face="normal" font="default" size="100%">Ju, Xiu-Lian</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Liu, Gen-Yan</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Homology modeling of human alpha 1 beta 2 gamma 2 and house fly beta 3 GABA receptor channels and Surflex-docking of fipronil.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of molecular modeling</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">fipronil</style></keyword><keyword><style  face="normal" font="default" size="100%">homology modeling</style></keyword><keyword><style  face="normal" font="default" size="100%">house fly beta 3 GABA receptor</style></keyword><keyword><style  face="normal" font="default" size="100%">human alpha 1 beta 2 gamma 2 GABAA receptor</style></keyword><keyword><style  face="normal" font="default" size="100%">selectivity</style></keyword><keyword><style  face="normal" font="default" size="100%">surflex-docking</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2009</style></year><pub-dates><date><style  face="normal" font="default" size="100%">09/2009</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/19238461</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">15</style></volume><pages><style face="normal" font="default" size="100%">1145–1153</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">To further explore the mechanism of selective binding of the representative gamma-aminobutyric acid receptors (GABARs) noncompetitive antagonist (NCA) fipronil to insect over mammalian GABARs, three-dimensional models of human alpha 1 beta 2 gamma 2 and house fly beta 3 GABAR were generated by homology modeling, using the cryo-electron microscopy structure of the nicotinic acetylcholine receptor (nAChR) of Torpedo marmorata as a template. Fipronil was docked into the putative binding site of the human alpha 1 beta 2 gamma 2 and house fly beta 3 receptors by Surflex-docking, and the calculated docking energies are in agreement with experimental results. The GABA receptor antagonist fipronil exhibited higher potency with house fly beta 3 GABAR than with human alpha 1 beta 2 gamma 2 GABAR. Furthermore, analyses of Surflex-docking suggest that the H-bond interaction of fipronil with Ala2 and Thr6 in the second transmembrane segment (TM2) of these GABARs plays a relatively important role in ligand selective binding. The different subunit assemblies of human alpha 1 beta 2 gamma 2 and house fly beta 3 GABARs may result in differential selectivity for fipronil.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Wang, Yu</style></author><author><style face="normal" font="default" size="100%">Pillai, Shreejith</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">H-reflex down-conditioning greatly increases the number of identifiable GABAergic interneurons in rat ventral horn.</style></title><secondary-title><style face="normal" font="default" size="100%">Neuroscience letters</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">activity-dependent plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">GABAergic interneurons</style></keyword><keyword><style  face="normal" font="default" size="100%">H-reflex conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">learning and memory</style></keyword><keyword><style  face="normal" font="default" size="100%">Motor control</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2009</style></year><pub-dates><date><style  face="normal" font="default" size="100%">03/2009</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/19383426</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">452</style></volume><pages><style face="normal" font="default" size="100%">124–129</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">H-reflex down-conditioning increases GABAergic terminals on spinal cord motoneurons. To explore the origins of these terminals, we studied the numbers and distributions of spinal cord GABAergic interneurons. The number of identifiable GABAergic interneurons in the ventral horn was 78% greater in rats in which down-conditioning was successful than in naive rats or rats in which down-conditioning failed. No increase occurred in other spinal lamina or on the contralateral side. This finding supports the hypothesis that the corticospinal tract influence that induces the motoneuron plasticity underlying down-conditioning reaches the motoneuron through GABAergic interneurons in the ventral horn.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Pillai, Shreejith</style></author><author><style face="normal" font="default" size="100%">Wang, Yu</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Effects of H-reflex up-conditioning on GABAergic terminals on rat soleus motoneurons.</style></title><secondary-title><style face="normal" font="default" size="100%">The European journal of neuroscience</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">activity-dependent plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">Learning</style></keyword><keyword><style  face="normal" font="default" size="100%">Memory</style></keyword><keyword><style  face="normal" font="default" size="100%">Motor control</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">08/2008</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/18657184</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">28</style></volume><pages><style face="normal" font="default" size="100%">668–674</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">To explore the role of spinal cord plasticity in motor learning, we evaluated the effects of H-reflex operant conditioning on GABAergic input to rat spinal motoneurons. Previous work indicated that down-conditioning of soleus H-reflex increases GABAergic input to soleus motoneurons. This study explored the effect of H-reflex up-conditioning on GABAergic input. Of nine rats exposed to H-reflex up-conditioning, up-conditioning was successful (H-reflex increase &gt;or= 20%) in seven and failed (change &lt; 20%) in two. These rats and eight naive control (i.e. unconditioned) rats were injected with cholera toxin subunit B-conjugated Alexa fluor 488 into the soleus muscle to retrogradely label soleus motoneurons. Sections containing soleus motoneurons were processed for GAD(67) [one of the two principal forms of the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD)] with an ABC-peroxidase system. Two blinded independent raters counted and measured GABAergic terminals on these motoneurons. Unlike successful down-conditioning, which greatly increased the number of identifiable GABAergic terminals on the motoneurons, up-conditioning did not significantly change GABAergic terminal number. Successful up-conditioning did produce slight but statistically significant increases in GABAergic terminal diameter and soma coverage. These results are consistent with other data indicating that up- and down-conditioning are not mirror images of each other, but rather have different mechanisms. Although the marked changes in GABAergic terminals with down-conditioning probably contribute to H-reflex decrease, the modest changes in GABAergic terminals associated with up-conditioning may be compensatory or reactive plasticity, rather than the plasticity responsible for H-reflex increase. As a variety of spinal and supraspinal GABAergic neurons innervate motoneurons, the changes found with up-conditioning may be in terminals other than those affected in successful down-conditioning.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Tennissen, Ann M.</style></author><author><style face="normal" font="default" size="100%">Mongeluzi, Donna L.</style></author><author><style face="normal" font="default" size="100%">Dudek, Christopher J.</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">An in vitro protocol for recording from spinal motoneurons of adult rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Tissue and Organ Harvesting</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">07/2008</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/18463177</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">100</style></volume><pages><style face="normal" font="default" size="100%">474–481</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">In vitro slice preparations of CNS tissue are invaluable for studying neuronal function. However, up to now, slice protocols for adult mammal spinal motoneurons–the final common pathway for motor behaviors–have been available for only limited portions of the spinal cord. In most cases, these preparations have not been productive due to the poor viability of motoneurons in vitro. This report describes and validates a new slice protocol that for the first time provides reliable intracellular recordings from lumbar motoneurons of adult rats. The key features of this protocol are: preexposure to 100% oxygen; laminectomy prior to perfusion; anesthesia with ketamine/xylazine; embedding the spinal cord in agar prior to slicing; and, most important, brief incubation of spinal cord slices in a 30% solution of polyethylene glycol to promote resealing of the many motoneuron dendrites cut during sectioning. Together, these new features produce successful recordings in 76% of the experiments and an average action potential amplitude of 76 mV. Motoneuron properties measured in this new slice preparation (i.e., voltage and current thresholds for action potential initiation, input resistance, afterhyperpolarization size and duration, and onset and offset firing rates during current ramps) are comparable to those recorded in vivo. Given the mechanical stability and precise control over the extracellular environment afforded by an in vitro preparation, this new protocol can greatly facilitate electrophysiological and pharmacological study of these uniquely important neurons and other delicate neuronal populations in adult mammals.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">English, Arthur W.</style></author><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Recovery of electromyographic activity after transection and surgical repair of the rat sciatic nerve.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Tibial Nerve</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2007</style></year><pub-dates><date><style  face="normal" font="default" size="100%">02/2007</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/17122310</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">97</style></volume><pages><style face="normal" font="default" size="100%">1127–1134</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The recovery of soleus (SOL), gastrocnemius (GAS), and tibialis anterior (TA) electromyographic activity (EMG) after transection and surgical repair of the sciatic nerve was studied in Sprague-Dawley rats using chronically implanted stimulation and recording electrodes. Spontaneous EMG activity in SOL and GAS and direct muscle (M) responses to posterior tibial nerve stimulation persisted for &lt; or =2 days after sciatic nerve transection, but SOL and GAS H-reflexes disappeared immediately. Spontaneous EMG activity began to return 2-3 wk after transection, rose nearly to pretransection levels by 60 days, and persisted for the duration of the study period (120 days). Recovery of stimulus-evoked EMG responses began about 30 days after sciatic nerve transection as multiple small responses with a wide range of latencies. Over time, the latencies of these fractionated responses shortened, their amplitudes increased, and they merged into a distinct short-latency component (the putative M response) and a distinct long-latency component (the putative H-reflex). The extent of recovery of stimulation-evoked EMG was modest: even 100 days after sciatic nerve transection, the responses were still much smaller than those before transection. Similar gradual development of responses to posterior tibial nerve stimulation was also seen in TA, suggesting that some regenerating fibers sent branches into both tibial and common peroneal nerves.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Pillai, Shreejith</style></author><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Wang, Yu</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Spinal and supraspinal effects of long-term stimulation of sensorimotor cortex in rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Time Factors</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2007</style></year><pub-dates><date><style  face="normal" font="default" size="100%">08/2007</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/17522179</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">98</style></volume><pages><style face="normal" font="default" size="100%">878–887</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Sensorimotor cortex (SMC) modifies spinal cord reflex function throughout life and is essential for operant conditioning of the H-reflex. To further explore this long-term SMC influence over spinal cord function and its possible clinical uses, we assessed the effect of long-term SMC stimulation on the soleus H-reflex. In freely moving rats, the soleus H-reflex was measured 24 h/day for 12 wk. The soleus background EMG and M response associated with H-reflex elicitation were kept stable throughout. SMC stimulation was delivered in a 20-day-on/20-day-off/20-day-on protocol in which a train of biphasic 1-ms pulses at 25 Hz for 1 s was delivered every 10 s for the on-days. The SMC stimulus was automatically adjusted to maintain a constant descending volley. H-reflex size gradually increased during the 20 on-days, stayed high during the 20 off-days, and rose further during the next 20 on-days. In addition, the SMC stimulus needed to maintain a stable descending volley rose steadily over days. It fell during the 20 off-days and rose again when stimulation resumed. These results suggest that SMC stimulation, like H-reflex operant conditioning, induces activity-dependent plasticity in both the brain and the spinal cord and that the plasticity responsible for the H-reflex increase persists longer after the end of SMC stimulation than that underlying the change in the SMC response to stimulation.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The cerebellum in maintenance of a motor skill: a hierarchy of brain and spinal cord plasticity underlies H-reflex conditioning.</style></title><secondary-title><style face="normal" font="default" size="100%">Learning &amp; memory (Cold Spring Harbor, N.Y.)</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">03/2006</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16585796</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">13</style></volume><pages><style face="normal" font="default" size="100%">208–215</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Operant conditioning of the H-reflex, the electrical analog of the spinal stretch reflex, is a simple model of skill acquisition and involves plasticity in the spinal cord. Previous work showed that the cerebellum is essential for down-conditioning the H-reflex. This study asks whether the cerebellum is also essential for maintaining down-conditioning. After rats decreased the soleus H-reflex over 50 d in response to the down-conditioning protocol, the cerebellar output nuclei dentate and interpositus (DIN) were ablated, and down-conditioning continued for 50-100 more days. In naive (i.e., unconditioned) rats, DIN ablation itself has no significant long-term effect on H-reflex size. During down-conditioning prior to DIN ablation, eight Sprague-Dawley rats decreased the H-reflex to 57% (+/-4 SEM) of control. It rose after ablation, stabilizing within 2 d at about 75% and remaining there until approximately 40 d after ablation. It then rose to approximately 130%, where it remained through the end of study 100 d after ablation. Thus, DIN ablation in down-conditioned rats caused an immediate increase and a delayed increase in the H-reflex. The final result was an H-reflex significantly larger than that prior to down-conditioning. Combined with previous work, these remarkable results suggest that the spinal cord plasticity directly responsible for down-conditioning, which survives only 5-10 d on its own, is maintained by supraspinal plasticity that survives approximately 40 d after loss of cerebellar output. Thus, H-reflex conditioning seems to depend on a hierarchy of brain and spinal cord plasticity to which the cerebellum makes an essential contribution.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Tennissen, Ann M.</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Corticospinal tract transection permanently abolishes H-reflex down-conditioning in rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurotrauma</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">corticospinal tract</style></keyword><keyword><style  face="normal" font="default" size="100%">H-reflex conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">rat</style></keyword><keyword><style  face="normal" font="default" size="100%">spinal cord injury</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">11/2006</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/17115915</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">23</style></volume><pages><style face="normal" font="default" size="100%">1705–1712</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Previous studies have shown that corticospinal tract (CST) transection, but not transection of other major spinal cord tracts, prevents down-conditioning of the H-reflex, the electrical analog of the spinal stretch reflex. This study set out to determine whether the loss of the capacity for H-reflex down-conditioning caused by CST transection is permanent. Female Sprague-Dawley rats received CST, lateral column (LC), or dorsal column ascending tract (DA) transection at T8-9; 9-10 months later, they were exposed to the H-reflex down-conditioning protocol for 50 days. In the LC and DA rats, H-reflex size fell to 60 (+/- 9 SEM)% and 60 (+/- 19)%, respectively, of its initial size. This down-conditioning was comparable to that of normal rats. In contrast, H-reflex size in the CST rats rose to 170 (+/- 42)% of its initial size. A similar rise does not occur in rats exposed to down-conditioning shortly after CST transection. These results indicate that CST transection permanently eliminates the capacity for H-reflex down-conditioning and has gradual long-term effects on sensorimotor cortex function. They imply that H-reflex down-conditioning can be a reliable measure of CST function for long-term studies of the effects of spinal cord injury and/or for evaluations of the efficacy of experimental therapeutic procedures, such as those intended to promote CST regeneration. The results also suggest that the role of sensorimotor cortex in down-conditioning extends beyond generation of the essential CST activity.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Tennissen, Ann M.</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Diurnal H-reflex variation in mice.</style></title><secondary-title><style face="normal" font="default" size="100%">Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">circadian rhythm</style></keyword><keyword><style  face="normal" font="default" size="100%">Electromyography</style></keyword><keyword><style  face="normal" font="default" size="100%">implanted electrodes</style></keyword><keyword><style  face="normal" font="default" size="100%">Monosynaptic</style></keyword><keyword><style  face="normal" font="default" size="100%">Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">01/2006</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16151781</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">168</style></volume><pages><style face="normal" font="default" size="100%">517–528</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Mice exhibit diurnal variation in complex motor behaviors, but little is known about diurnal variation in simple spinally mediated functions. This study describes diurnal variation in the H-reflex (HR), a wholly spinal and largely monosynaptic reflex. Six mice were implanted with tibial nerve cuff electrodes and electrodes in the soleus and gastrocnemius muscles, for recording of ongoing and nerve-evoked electromyographic activity (EMG). Stimulation and recording were under computer control 24 h/day. During a 10-day recording period, HR amplitude varied throughout the day, usually being larger in the dark than in the light. This diurnal HR variation could not be attributed solely to differences in the net ongoing level of descending and segmental excitation to the spinal cord or stimulus intensity. HRs were larger in the dark than in the light even after restricting the evoked responses to subsets of trials having similar ongoing EMG and M-responses. The diurnal variation in the HR was out of phase with that reported previously for rats, but was in phase with that observed in monkeys. These data, supported by those in other species, suggest that the supraspinal control of the excitability of the HR pathway varies throughout the day in a species-specific pattern. This variation should be taken into account in experimental and clinical studies of spinal reflexes recorded at different times of day.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Tennissen, Ann M.</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">H-reflex operant conditioning in mice.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">10/2006</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16837659</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">96</style></volume><pages><style face="normal" font="default" size="100%">1718–1727</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Rats, monkeys, and humans can alter the size of their spinal stretch reflex and its electrically induced analog, the H-reflex (HR), when exposed to an operant conditioning paradigm. Because this conditioning induces plasticity in the spinal cord, it offers a unique opportunity to identify the neuronal sites and mechanisms that underlie a well-defined change in a simple behavior. To facilitate these studies, we developed an HR operant conditioning protocol in mice, which are better suited to genetic manipulation and electrophysiological spinal cord study in vitro than rats or primates. Eleven mice under deep surgical anesthesia were implanted with tibial nerve stimulating electrodes and soleus and gastrocnemius intramuscular electrodes for recording ongoing and stimulus-evoked EMG activity. During the 24-h/day computer-controlled experiment, mice received a liquid reward for either increasing (up-conditioning) or decreasing (down-conditioning) HR amplitude while maintaining target levels of ongoing EMG and directly evoked EMG (M-responses). After 3-7 wk of conditioning, the HR amplitude was 133 +/- 7% (SE) of control for up-conditioning and 71 +/- 8% of control for down-conditioning. HR conditioning was successful (i.e., &gt; or =20% change in HR amplitude in the appropriate direction) in five of six up-conditioned animals (mean final HR amplitude = 139 +/- 5% of control HR for successful mice) and in four of five down-conditioned animals (mean final HR amplitude = 63 +/- 8% of control HR for successful mice). These effects were not attributable to differences in the net level of motoneuron pool excitation, stimulation strength, or distribution of HR trials throughout the day. Thus mice exhibit HR operant conditioning comparable with that observed in rats and monkeys.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Thompson, Aiko K.</style></author><author><style face="normal" font="default" size="100%">Stein, Richard B.</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Modulation in spinal circuits and corticospinal connections following nerve stimulation and operant conditioning.</style></title><secondary-title><style face="normal" font="default" size="100%">Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Conference</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">09/2006</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/17946939</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">1</style></volume><pages><style face="normal" font="default" size="100%">2138–2141</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Neural plasticity occurs throughout adult life. In healthy individuals, different spinal pathways are differently modulated during different daily activities. Drastic changes to nervous system activity and connections caused by injuries or diseases alter spinal reflexes, and this is often related to disturbed motor functions. In both health and disease, spinal reflexes are subject to substantial modifications. Plasticity in supraspinal descending connections is even more remarkable; corticospinal connectivity has been shown to be extremely plastic. In this session, we describe two approaches for possibly improving recovery after central nervous system (CNS) lesions. They are very different, but both involve repetitive nerve stimulation and CNS plasticity. The first approach is functional electrical stimulation (FES) of the common peroneal nerve, which has been used to treat foot drop in patients with CNS lesions. The second approach is operant conditioning of a spinal reflex. Spinal reflex operant conditioning studies in animal models have shown plastic changes in spinal cord neurons associated with this form of learning and improved locomotor function in incomplete spinal cord injured rats. Thus, reflex conditioning might be a robust approach to inducing plasticity at spinal and supraspinal levels. As a first step in establishing this approach and characterizing its effects in the human adult CNS, we are currently investigating the extent and time course of operant conditioning of the soleus H-reflex in healthy subjects. In results to date, all subjects (n=5) have changed reflex size in the correct direction to various degree (16-36%) over 2-3 months of conditioning, indicating possibility that H-reflex conditioning can occur in humans. At the same time, the substantial inter-subject variation in the time course and extent of conditioning suggest that additional data are needed to establish its principal features. We hope that studying modulation and modification o- f the CNS by different approaches will help us further understand the plasticity of the human adult nervous system.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Wang, Yu</style></author><author><style face="normal" font="default" size="100%">Pillai, Shreejith</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Motor learning changes GABAergic terminals on spinal motoneurons in normal rats.</style></title><secondary-title><style face="normal" font="default" size="100%">The European journal of neuroscience</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">activity-dependent plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">GABA</style></keyword><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">Memory</style></keyword><keyword><style  face="normal" font="default" size="100%">Motor control</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">01/2006</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16420424</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">23</style></volume><pages><style face="normal" font="default" size="100%">141–150</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The role of spinal cord plasticity in motor learning is largely unknown. This study explored the effects of H-reflex operant conditioning, a simple model of motor learning, on GABAergic input to spinal motoneurons in rats. Soleus motoneurons were labeled by retrograde transport of a fluorescent tracer and GABAergic terminals on them were identified by glutamic acid decarboxylase (GAD)67 immunoreactivity. Three groups were studied: (i) rats in which down-conditioning had reduced the H-reflex (successful HRdown rats); (ii) rats in which down-conditioning had not reduced the H-reflex (unsuccessful HRdown rats) and (iii) unconditioned (naive) rats. The number, size and GAD density of GABAergic terminals, and their coverage of the motoneuron, were significantly greater in successful HRdown rats than in unsuccessful HRdown or naive rats. It is likely that these differences are due to modifications in terminals from spinal interneurons in lamina VI-VII and that the increased terminal number, size, GAD density and coverage in successful HRdown rats reflect and convey a corticospinal tract influence that changes motoneuron firing threshold and thereby decreases the H-reflex. GABAergic terminals in spinal cord change after spinal cord transection. The present results demonstrate that such spinal cord plasticity also occurs in intact rats in the course of motor learning and suggest that this plasticity contributes to skill acquisition.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jakeman, Lyn B.</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Stokes, Bradford T.</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Operant conditioning of H-reflex can correct a locomotor abnormality after spinal cord injury in rats.</style></title><secondary-title><style face="normal" font="default" size="100%">The Journal of neuroscience : the official journal of the Society for Neuroscience</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">H-reflex conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">Learning</style></keyword><keyword><style  face="normal" font="default" size="100%">Locomotion</style></keyword><keyword><style  face="normal" font="default" size="100%">Memory</style></keyword><keyword><style  face="normal" font="default" size="100%">Motor control</style></keyword><keyword><style  face="normal" font="default" size="100%">Rehabilitation</style></keyword><keyword><style  face="normal" font="default" size="100%">spinal cord injury</style></keyword><keyword><style  face="normal" font="default" size="100%">spinal cord plasticity</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">11/2006</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/17135415</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">26</style></volume><pages><style face="normal" font="default" size="100%">12537–12543</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;This study asked whether operant conditioning of the H-reflex can modify locomotion in spinal cord-injured rats. Midthoracic transection of the right lateral column of the spinal cord produced a persistent asymmetry in the muscle activity underlying treadmill locomotion. The rats were then either exposed or not exposed to an H-reflex up-conditioning protocol that greatly increased right soleus motoneuron response to primary afferent input, and locomotion was reevaluated. H-reflex up-conditioning increased the right soleus burst and corrected the locomotor asymmetry. In contrast, the locomotor asymmetry persisted in the control rats. These results suggest that appropriately selected reflex conditioning protocols might improve function in people with partial spinal cord injuries. Such protocols might be especially useful when significant regeneration becomes possible and precise methods for reeducating the regenerated spinal cord neurons and synapses are needed for restoring effective function.&lt;/p&gt;</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Operant conditioning of reciprocal inhibition in rat soleus muscle.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">Stretch</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">10/2006</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16807351</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">96</style></volume><pages><style face="normal" font="default" size="100%">2144–2150</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Operant conditioning of the H-reflex, the electrical analog of the spinal stretch reflex (SSR), induces activity-dependent plasticity in the spinal cord and might be used to improve locomotion after spinal cord injury. To further assess the potential clinical significance of spinal reflex conditioning, this study asks whether another well-defined spinal reflex pathway, the disynaptic pathway underlying reciprocal inhibition (RI), can also be operantly conditioned. Sprague-Dawley rats were implanted with electromyographic (EMG) electrodes in right soleus (SOL) and tibialis anterior (TA) muscles and a stimulating cuff on the common peroneal (CP) nerve. When background EMG in both muscles remained in defined ranges, CP stimulation elicited the TA H-reflex and SOL RI. After collection of control data for 20 days, each rat was exposed for 50 days to up-conditioning (RIup mode) or down-conditioning (RIdown mode) in which food reward occurred if SOL RI evoked by CP stimulation was more (RIup mode) or less (RIdown mode) than a criterion. TA and SOL background EMG and TA M response remained stable. In every rat, RI conditioning was successful (i.e., change &gt; or =20% in the correct direction). In the RIup rats, final SOL RI averaged 171+/- 28% (mean +/- SE) of control, and final TA H-reflex averaged 114 +/- 14%. In the RIdown rats, final SOL RI averaged 37 +/- 13% of control, and final TA H-reflex averaged 60 +/- 18%. Final SOL RI and TA H-reflex sizes were significantly correlated. Thus like the SSR and the H-reflex, RI can be operantly conditioned; and conditioning one reflex can affect another reflex as well.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Sensorimotor cortex ablation prevents H-reflex up-conditioning and causes a paradoxical response to down-conditioning in rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Somatosensory Cortex</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">07/2006</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16598062</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">96</style></volume><pages><style face="normal" font="default" size="100%">119–127</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Operant conditioning of the H-reflex, a simple model for skill acquisition, requires the corticospinal tract (CST) and does not require other major descending pathways. To further explore its mechanisms, we assessed the effects of ablating contralateral sensorimotor cortex (cSMC). In 22 Sprague-Dawley rats, the hindlimb area of left cSMC was ablated. EMG electrodes were implanted in the right soleus muscle and a stimulating cuff was placed around the right posterior tibial nerve. When EMG remained in a specified range, nerve stimulation just above the M response threshold elicited the H-reflex. In control mode, no reward occurred. In conditioning mode, reward occurred if H-reflex size was above (HRup mode) or below (HRdown mode) a criterion value. After exposure to the control mode for &gt; or = 10 days, each rat was exposed for another 50 days to the control mode, the HRup mode, or the HRdown mode. In control and HRup rats, final H-reflex size was not significantly different from initial H-reflex size. In contrast, in HRdown rats, final H-reflex size was significantly increased to an average of 136% of initial size. Thus like recent CST transection, cSMC ablation greatly impaired up-conditioning. However, unlike recent CST transection, cSMC produced a paradoxical response to down-conditioning: the H-reflex actually increased. These results confirm the critical role of cSMC in H-reflex conditioning and suggest that this role extends beyond producing essential CST activity. Its interactions with ipsilateral SMC or other areas contribute to the complex pattern of spinal and supraspinal plasticity that underlies H-reflex conditioning.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Ablation of cerebellar nuclei prevents H-reflex down-conditioning in rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Learning &amp; memory (Cold Spring Harbor, N.Y.)</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">Vestibulo-Ocular</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2005</style></year><pub-dates><date><style  face="normal" font="default" size="100%">05/2005</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/15930503</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">12</style></volume><pages><style face="normal" font="default" size="100%">248–254</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">While studies of cerebellar involvement in learning and memory have described plasticity within the cerebellum, its role in acquisition of plasticity elsewhere in the CNS is largely unexplored. This study set out to determine whether the cerebellum is needed for acquisition of the spinal cord plasticity that underlies operantly conditioned decrease in the H-reflex, the electrical analog of the spinal stretch reflex. Rats in which the cerebellar output nuclei dentate and interpositus (DIN) had been ablated were exposed for 50 d to the H-reflex down-conditioning protocol. DIN ablation, which in itself had no significant long-term effect on H-reflex size, entirely prevented acquisition of a smaller H-reflex. Since previous studies show that corticospinal tract (CST) transection also prevents down-conditioning while transection of the rubrospinal tract and other major descending tracts does not, this result implies that DIN output that affects cortex is essential for generation of the CST activity that induces the spinal cord plasticity, which is, in turn, directly responsible for the smaller H-reflex. The result extends the role of the cerebellum in learning and memory to include participation in induction of plasticity elsewhere in the CNS, specifically in the spinal cord. The cerebellum might simply support processes in sensorimotor cortex or elsewhere that change the spinal cord, or the cerebellum itself might undergo plasticity similar to that occurring with vestibulo-ocular reflex (VOR) or eyeblink conditioning.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jakeman, Lyn B.</style></author><author><style face="normal" font="default" size="100%">Gerwin Schalk</style></author><author><style face="normal" font="default" size="100%">Stokes, Bradford T.</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The interaction of a new motor skill and an old one: H-reflex conditioning and locomotion in rats.</style></title><secondary-title><style face="normal" font="default" size="100%">The Journal of neuroscience : the official journal of the Society for Neuroscience</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">H-reflex conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">Learning</style></keyword><keyword><style  face="normal" font="default" size="100%">Locomotion</style></keyword><keyword><style  face="normal" font="default" size="100%">memory consolidation</style></keyword><keyword><style  face="normal" font="default" size="100%">Motor control</style></keyword><keyword><style  face="normal" font="default" size="100%">Rehabilitation</style></keyword><keyword><style  face="normal" font="default" size="100%">spinal cord plasticity</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2005</style></year><pub-dates><date><style  face="normal" font="default" size="100%">07/2005</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16033899</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">25</style></volume><pages><style face="normal" font="default" size="100%">6898–6906</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">New and old motor skills can interfere with each other or interact in other ways. Because each skill entails a distributed pattern of activity-dependent plasticity, investigation of their interactions is facilitated by simple models. In a well characterized model of simple learning, rats and monkeys gradually change the size of the H-reflex, the electrical analog of the spinal stretch reflex. This study evaluates in normal rats the interactions of this new skill of H-reflex conditioning with the old well established skill of overground locomotion. In rats in which the soleus H-reflex elicited in the conditioning protocol (i.e., the conditioning H-reflex) had been decreased by down-conditioning, the H-reflexes elicited during the stance and swing phases of locomotion (i.e., the locomotor H-reflexes) were also smaller. Similarly, in rats in which the conditioning H-reflex had been increased by up-conditioning, the locomotor H-reflexes were also larger. Soleus H-reflex conditioning did not affect the duration, length, or right/left symmetry of the step cycle. However, the conditioned change in the stance H-reflex was positively correlated with change in the amplitude of the soleus locomotor burst, and the correlation was consistent with current estimates of the contribution of primary afferent input to the burst. Although H-reflex conditioning and locomotion did not interfere with each other, H-reflex conditioning did affect how locomotion was produced: it changed soleus burst amplitude and may have induced compensatory changes in the activity of other muscles. These results illustrate and clarify the subtlety and complexity of skill interactions. They also suggest that H-reflex conditioning might be used to improve the abnormal locomotion produced by spinal cord injury or other disorders of supraspinal control.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Tennissen, Ann M.</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Gerwin Schalk</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Long-term spinal reflex studies in awake behaving mice.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neuroscience methods</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Electromyography</style></keyword><keyword><style  face="normal" font="default" size="100%">implanted electrodes</style></keyword><keyword><style  face="normal" font="default" size="100%">Monosynaptic</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2005</style></year><pub-dates><date><style  face="normal" font="default" size="100%">12/2005</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16026848</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">149</style></volume><pages><style face="normal" font="default" size="100%">134–143</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The increasing availability of genetic variants of mice has facilitated studies of the roles of specific molecules in specific behaviors. The contributions of such studies could be strengthened and extended by correlation with detailed information on the patterns of motor commands throughout the course of specific behaviors in freely moving animals. Previously reported methodologies for long-term recording of electromyographic activity (EMG) in mice using implanted electrodes were designed for intermittent, but not continuous operation. This report describes the fabrication, implantation, and utilization of fine wire electrodes for continuous long-term recordings of spontaneous and nerve-evoked EMG in mice. Six mice were implanted with a tibial nerve cuff electrode and EMG electrodes in soleus and gastrocnemius muscles. Wires exited through a skin button and traveled through an armored cable to an electrical commutator. In mice implanted for 59-144 days, ongoing EMG was monitored continuously (i.e., 24 h/day, 7 days/week) by computer for 18-92 days (total intermittent recording for 25-130 days). When the ongoing EMG criteria were met, the computer applied the nerve stimulus, recorded the evoked EMG response, and determined the size of the M-response (MR) and the H-reflex (HR). It continually adjusted stimulation intensity to maintain a stable MR size. Stable recordings of ongoing EMG, MR, and HR were obtained typically 3 weeks after implantation. This study demonstrates the feasibility of long-term continuous EMG recordings in mice for addressing a variety of neurophysiological and behavioral issues.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Conditioned H-reflex increase persists after transection of the main corticospinal tract in rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Spinal Cord Injuries</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2003</style></year><pub-dates><date><style  face="normal" font="default" size="100%">11/2003</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/12917382</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">90</style></volume><pages><style face="normal" font="default" size="100%">3572–3578</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The brain shapes spinal cord function throughout life. Operant conditioning of the H-reflex, the electrical analog of the spinal stretch reflex (SSR), is a relatively simple model for exploring the spinal cord plasticity underlying this functional change and may provide a new method for modifying spinal cord reflexes after spinal cord injury. In response to an operant conditioning protocol, rats can gradually increase (i.e., up-training mode) or decrease (i.e., down-training mode) the soleus H-reflex. This study explored the effects of midthoracic transection of the ipsilateral lateral column (LC) (rubrospinal, vestibulospinal, and reticulospinal tracts), the dorsal column corticospinal tract (CST), or the dorsal column ascending tract (DA) on maintenance of an H-reflex increase that has already occurred. Rats were implanted with EMG electrodes in the right soleus muscle and a nerve-stimulating cuff on the right posterior tibial nerve. After initial (i.e., control) H-reflex size was determined, the rats were exposed for 50 days to the up-training mode, in which reward was given when the H-reflex was above a criterion value. H-reflex size gradually rose to 168 +/- 12% (mean +/- SE) of its initial value. Each rat then received an LC, CST, or DA transection and continued under the up-training mode for 50 more days. None of the transections abolished the H-reflex increase. H-reflex size increased further to 197 +/- 19% of its initial value and did not differ significantly among LC, CST, and DA rats (P &gt; 0.78 by ANOVA). Although earlier studies show that the main CST is needed for acquisition of H-reflex up-training and down-training and for maintenance of down-training, this study shows that it is not needed for maintenance of up-training. It adds to the evidence that H-reflex conditioning changes the spinal cord and that the spinal cord plasticity associated with up-training is different from that associated with down-training.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Corticospinal tract transection prevents operantly conditioned H-reflex increase in rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">dorsal column</style></keyword><keyword><style  face="normal" font="default" size="100%">lateral column</style></keyword><keyword><style  face="normal" font="default" size="100%">Learning</style></keyword><keyword><style  face="normal" font="default" size="100%">plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">spinal cord injury</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2002</style></year><pub-dates><date><style  face="normal" font="default" size="100%">05/2002</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/11976762</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">144</style></volume><pages><style face="normal" font="default" size="100%">88–94</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Operant conditioning of the H-reflex, the electrical analog of the spinal stretch reflex, in freely moving rats is a relatively simple model for studying long-term supraspinal control over spinal cord function. Motivated by food reward, rats can gradually increase (i.e., up-condition) or decrease (i.e., down-condition) the soleus H-reflex. Earlier work showed that corticospinal tract transection prevents acquisition and maintenance of H-reflex down-conditioning while transection of other major spinal cord tracts does not. This study explores the effects on acquisition of up-conditioning of the right soleus H-reflex of mid-thoracic transection of: the right lateral column (LC, five rats) (containing the rubrospinal, vestibulospinal, and reticulospinal tracts); the entire dorsal column (DC, six rats) [containing the main corticospinal tract (CST) and the dorsal ascending tract (DA)]; the CST alone (five rats); or the DA alone (seven rats). After initial (i.e., control) H-reflex amplitude was determined, the rat was exposed for 50 days to the up-conditioning mode in which reward was given when the H-reflex was above a criterion value. H-reflex amplitude at the end of up-conditioning was compared to initial H-reflex amplitude. An increase &gt; or =20% was defined as successful up-conditioning. In intact rats, H-reflex amplitude at the end of up-conditioning averaged 164% (+/-10%, SE), and 81% were successful. In the present study, LC and DA rats were similar to intact rats in final H-reflex amplitude and percent successful. In contrast, results for DC and CST rats were significantly different from those of intact rats. In the six DC rats, final H-reflex amplitude averaged 105% (+/-3)% of control and none was successful; and in the five CST rats, final H-reflex amplitude averaged 94% (+/-3)% and none was successful. The results indicate that the main CST, located in the dorsal column, is essential for H-reflex up-conditioning as it is for down-conditioning, while the dorsal column ascending tract and the ipsilateral lateral column (containing the main rubrospinal, vestibulospinal, and reticulospinal tracts) do not appear to be essential.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Jakeman, Lyn B.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Corticospinal tract transection reduces H-reflex circadian rhythm in rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Brain research</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">circadian rhythms</style></keyword><keyword><style  face="normal" font="default" size="100%">corticospinal tract</style></keyword><keyword><style  face="normal" font="default" size="100%">diurnal rhythm</style></keyword><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">rat</style></keyword><keyword><style  face="normal" font="default" size="100%">spinal cord injury</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2002</style></year><pub-dates><date><style  face="normal" font="default" size="100%">06/2002</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/12031858</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">942</style></volume><pages><style face="normal" font="default" size="100%">101–108</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">In freely moving rats and monkeys, H-reflex amplitude displays a marked circadian variation without change in background motoneuron tone. In rats, the H-reflex is largest around noon and smallest around midnight. The present study evaluated in rats the effects on this rhythm of calibrated contusions of mid-thoracic spinal cord and mid-thoracic transection of specific spinal cord pathways. In 33 control rats, rhythm amplitude averaged 29.0(+/-2.6 S.E.)% of H-reflex amplitude. Contusion injuries at T8-9 that destroyed 53-88% of the white matter significantly reduced the rhythm to 18.9(+/-2.4)% of H-reflex amplitude. Transection of the ipsilateral lateral column, which contains the rubrospinal, vestibulospinal, and reticulospinal tracts, or bilateral transection of the dorsal column ascending tract did not affect rhythm amplitude or phase. In contrast, bilateral transection of the main corticospinal tract significantly reduced the rhythm to 14.7(+/-6.6)%. These results indicate that the H-reflex circadian rhythm depends in part on descending influence from the brain and that this influence is conveyed by the main corticospinal tract.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Probable corticospinal tract control of spinal cord plasticity in the rat.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Spinal Cord Injuries</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2002</style></year><pub-dates><date><style  face="normal" font="default" size="100%">02/2002</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/11826033</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">87</style></volume><pages><style face="normal" font="default" size="100%">645–652</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Descending activity from the brain shapes spinal cord reflex function throughout life, yet the mechanisms responsible for this spinal cord plasticity are poorly understood. Operant conditioning of the H-reflex, the electrical analogue of the spinal stretch reflex, is a simple model for investigating these mechanisms. An earlier study in the Sprague-Dawley rat showed that acquisition of an operantly conditioned decrease in the soleus H-reflex is not prevented by mid-thoracic transection of the ipsilateral lateral column (LC), which contains the rubrospinal, reticulospinal, and vestibulospinal tracts, and is prevented by transection of the dorsal column, which contains the main corticospinal tract (CST) and the dorsal column ascending tract (DA). The present study explored the effects of CST or DA transection on acquisition of an H-reflex decrease, and the effects of LC, CST, or DA transection on maintenance of an established decrease. CST transection prior to conditioning prevented acquisition of H-reflex decrease, while DA transection did not do so. CST transection after H-reflex decrease had been acquired led to gradual loss of the decrease over 10 days, and resulted in an H-reflex that was significantly larger than the original, naive H-reflex. In contrast, LC or DA transection after H-reflex decrease had been acquired did not affect maintenance of the decrease. These results, in combination with the earlier study, strongly imply that in the rat the corticospinal tract (CST) is essential for acquisition and maintenance of operantly conditioned decrease in the H-reflex and that other major spinal cord pathways are not essential. This previously unrecognized aspect of CST function gives insight into the processes underlying acquisition and maintenance of motor skills and could lead to novel methods for inducing, guiding, and assessing recovery of function after spinal cord injury.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Sheikh, H.</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Effects of chronic nerve cuff and intramuscular electrodes on rat triceps surae motor units.</style></title><secondary-title><style face="normal" font="default" size="100%">Neuroscience letters</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">chronic recording</style></keyword><keyword><style  face="normal" font="default" size="100%">contraction time</style></keyword><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">implanted electrodes</style></keyword><keyword><style  face="normal" font="default" size="100%">motor units</style></keyword><keyword><style  face="normal" font="default" size="100%">nerve cuff</style></keyword><keyword><style  face="normal" font="default" size="100%">reinnervation</style></keyword><keyword><style  face="normal" font="default" size="100%">sag</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2001</style></year><pub-dates><date><style  face="normal" font="default" size="100%">10/2001</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/11578831</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">312</style></volume><pages><style face="normal" font="default" size="100%">1–4</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">In order to assess the long-term effects of implanted electrodes on motor unit properties, we studied triceps surae (TS) motor units in rats implanted for 3-10 months with a tibial nerve cuff electrode for H-reflex elicitation and intramuscular electrodes for recording TS electromyographic activity. Motor units with sag from implanted rats displayed greater tetanic force than those from unimplanted rats. Motor units without sag had shorter twitch contraction times. This disrupted the relationship between sag and contraction time that was always present in unimplanted rats. These differences were consistent with a small degree of muscle denervation and subsequent reinnervation. Further analyses ascribed this effect to the nerve cuff rather than to the intramuscular electrodes. Comparable changes in motor unit properties may occur in humans with implanted nerve cuffs.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Sheikh, H.</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Motor unit properties after operant conditioning of rat H-reflex.</style></title><secondary-title><style face="normal" font="default" size="100%">Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">motor unit type</style></keyword><keyword><style  face="normal" font="default" size="100%">operant conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">triceps surae</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2001</style></year><pub-dates><date><style  face="normal" font="default" size="100%">10/2001</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/11681314</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">140</style></volume><pages><style face="normal" font="default" size="100%">382–386</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Operant conditioning of the H-reflex produces plasticity at several sites in the spinal cord, including the motoneuron. This study assessed whether this spinal cord plasticity is accompanied by changes in motor unit contractile properties. Thirty-one adult male Sprague-Dawley rats implanted for chronic recording of triceps surae electromyographic activity and H-reflex elicitation were exposed for at least 40 days to HRup or HRdown training, in which reward occurred when the H-reflex was greater than (12 HRup rats) or less than (12 HRdown rats) a criterion value, or continued under the control mode in which the H-reflex was simply measured (7 HRcon rats). At the end of H-reflex data collection, rats were anesthetized and the contractile properties of 797 single triceps surae motor units activated by intraaxonal (or intramyelin) current injection were determined. Motor units were classified as S, FR, Fint, or FF on the basis of sag and fatigue properties. Maximum tetanic force and twitch contraction time were also measured. HRdown rats exhibited a significant increase in the fatigue index of fast-twitch motor units. This resulted in a significant decrease in the percentage of Fint motor units and a significant increase in that of FR motor units. HRup conditioning had no effect on fatigue index. Neither HRup nor HRdown conditioning affected maximum tetanic force or twitch contraction time. These data are consistent with the hypothesis that conditioning mode-specific change in motoneuron firing patterns causes activity-dependent change in muscle properties.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Sheikh, H.</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Operant conditioning of rat H-reflex affects motoneuron axonal conduction velocity.</style></title><secondary-title><style face="normal" font="default" size="100%">Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">conduction velocity</style></keyword><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">motoneuron</style></keyword><keyword><style  face="normal" font="default" size="100%">plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2001</style></year><pub-dates><date><style  face="normal" font="default" size="100%">01/2001</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/11206290</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">136</style></volume><pages><style face="normal" font="default" size="100%">269–273</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">This study assessed the effects of operant conditioning of the H-reflex on motoneuron axonal conduction velocity in the rat. After measurement of the control H-reflex size, rats were either exposed for at least 40 days to the HRup or HRdown conditioning mode, in which reward occurred only if the soleus H-reflex was greater than (HRup mode) or less than (HRdown mode) a criterion or continued under the control condition (HRcon mode) in which the H-reflex was simply measured. We then measured axonal conduction velocity of triceps surae motor units of HRup, HRdown, and HRcon rats by stimulating the axon in the ventral root and recording from the tibial nerve. Conduction velocity was 8% less in successful HRdown rats than in HRcon rats (P=0.02). Conduction velocity in HRup rats and unsuccessful HRdown rats was not significantly different from that in HRcon rats. Since recording bypassed the intra-spinal portion of the motoneuron, the change was clearly in the axon. This decrease was similar to the 6% decrease previously found in successful HRdown monkeys. Unsuccessful HRdown rats and monkeys did not show this decrease. This result suggests that the mechanism of HRdown conditioning is similar in rats and monkeys and provides further support for the hypothesis that HRdown conditioning decreases motoneuron excitability by producing a positive shift in firing threshold. While traditional theories of learning emphasize synaptic plasticity, neuronal plasticity may also contribute to operantly conditioned behavioral changes.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Operant conditioning of rat H-reflex: effects on mean latency and duration.</style></title><secondary-title><style face="normal" font="default" size="100%">Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">Memory</style></keyword><keyword><style  face="normal" font="default" size="100%">plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2001</style></year><pub-dates><date><style  face="normal" font="default" size="100%">01/2001</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/11206291</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">136</style></volume><pages><style face="normal" font="default" size="100%">274–279</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">We are currently studying the mechanisms of operantly conditioned changes in the H-reflex in the rat. Primate data suggest that H-reflex decrease is due to a positive shift in motoneuron firing threshold and a small decrease in the monosynaptic excitatory postsynaptic potential (EPSP), and that increase might be due to change in group-I oligosynaptic (especially disynaptic) input. To further evaluate the possibility of conditioned change in oligosynaptic input, we compared the mean latency (i.e., the average latency of the entire H-reflex) and the duration of control (i.e., pre-conditioning) H-reflexes with those of H-reflexes after up-conditioning or down-conditioning. Up-conditioning was associated with small, statistically significant increases in H-reflex mean latency [+0.11+/-0.05 (+/-SE) ms] and duration (+0.32+/-0.16 ms). The mean latency of the H-reflex increase (i.e., the part added to the H-reflex by up-conditioning) was 0.28+/-0.14 (+/-SE) ms greater than that of the control H-reflex. Down-conditioning had no significant effect on mean latency or duration. While these results indicate that operant conditioning does not greatly change H-reflex mean latency or duration, the effects detected with up-conditioning are consistent with the hypothesis that decreased inhibition, or increased excitation, by homonymous and heteronymous group-I oligosynaptic input contributes to the H-reflex increase produced by up-conditioning. Several other mechanisms might also account for these small effects.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Feng-Chen, K. C.</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Stark, D. M.</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Short-Term and medium-term effects of spinal cord tract transections on soleus H-reflex in freely moving rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurotrauma</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">corticospinal tract</style></keyword><keyword><style  face="normal" font="default" size="100%">dorsal column</style></keyword><keyword><style  face="normal" font="default" size="100%">dorsal column ascending tract</style></keyword><keyword><style  face="normal" font="default" size="100%">lateral column</style></keyword><keyword><style  face="normal" font="default" size="100%">rat</style></keyword><keyword><style  face="normal" font="default" size="100%">soleus activity</style></keyword><keyword><style  face="normal" font="default" size="100%">spinal cord injury</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2001</style></year><pub-dates><date><style  face="normal" font="default" size="100%">03/2001</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/11284551</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">18</style></volume><pages><style face="normal" font="default" size="100%">313–327</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Spinal cord function is normally influenced by descending activity from supraspinal structures. When injury removes or distorts this influence, function changes and spasticity and other disabling problems eventually appear. Understanding how descending activity affects spinal cord function could lead to new means for inducing, guiding, and assessing recovery after injury. In this study, we investigated the short-term and medium-term effects of spinal cord bilateral dorsal column (DC), unilateral (ipsilateral) lateral column (LC), bilateral dorsal column ascending tract (DA), or bilateral dorsal column corticospinal tract (CST) transection at vertebral level T8-T9 on the soleus H-reflex in freely moving rats. Data were collected continuously for 10-20 days before and for 20-155 days after bilateral DC (13 rats), DA (10 rats), CST (eight rats), or ipsilateral LC (seven rats) transection. Histological examination showed that transections were 98(+/- 3 SD)% complete for DC rats, 80(+/- 20)% complete for LC rats, 91(+/- 13 SD)% complete for DA rats, and 95(+/-13)% complete for CST rats. LC, CST, and DA transections produced an immediate (i.e., first-day) increase in H-reflex amplitude. LC transection also produced a small decrease in background activity in the first few posttransection days. Other than this small decrease, none of the transections produced evidence for the phenomenon of spinal shock. For all transections, all measures returned to or neared pretransection values within 2 weeks. DA and LC transections were associated with modest increase in H-reflex amplitude 1-3 months after transection. These medium-term effects must be taken into account when assessing transection effects on operant conditioning of the H-reflex. At the same time, the results are consistent with other evidence that, while H-reflex rate dependence and H-reflex operant conditioning are sensitive measures of spinal cord injury, the H-reflex itself is not.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Time course of H-reflex conditioning in the rat.</style></title><secondary-title><style face="normal" font="default" size="100%">Neuroscience letters</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">Learning</style></keyword><keyword><style  face="normal" font="default" size="100%">Memory</style></keyword><keyword><style  face="normal" font="default" size="100%">plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">rat</style></keyword><keyword><style  face="normal" font="default" size="100%">Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2001</style></year><pub-dates><date><style  face="normal" font="default" size="100%">04/2001</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/11290393</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">302</style></volume><pages><style face="normal" font="default" size="100%">85–88</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">This study sought to define the course of operantly conditioned change in the rat soleus H-reflex and to determine whether, like H-reflex conditioning and spinal stretch reflex conditioning in the monkey, it develops in distinct phases. Data from 33 rats in which the right soleus H-reflex was trained up (i.e. HRup mode) and 38 in which it was trained down (i.e. HRdown mode) were averaged to define the courses of H-reflex increase and decrease. In HRup rats, the H-reflex showed a large phase I increase within the first 2 days followed by gradual phase II increase that continued for weeks. In HRdown rats, the H-reflex appeared to show a small phase I decrease and then showed a gradual phase II decrease over weeks. In combination with other recent work, the data suggest that H-reflex conditioning begins with a rapid mode-appropriate alteration in corticospinal tract influence over the spinal arc of the H-reflex, which causes phase I change, and that the continuation of this altered influence induces gradual spinal cord plasticity that is responsible for phase II change. The results further establish the similarity of H-reflex conditioning in primates and rats. Thus, they encourage efforts to produce a single coherent model of the phenomenon based on data from the two species and indicate the potential clinical relevance of the rat data.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Jakeman, L. B.</style></author><author><style face="normal" font="default" size="100%">Stokes, B. T.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Operant conditioning of H-reflex increase in spinal cord–injured rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurotrauma</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">operant conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">rat</style></keyword><keyword><style  face="normal" font="default" size="100%">soleus muscle</style></keyword><keyword><style  face="normal" font="default" size="100%">spinal cord injury</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1999</style></year><pub-dates><date><style  face="normal" font="default" size="100%">02/1999</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/10098962</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">175–186</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Operant conditioning of the spinal stretch reflex or its electrical analog, the H-reflex, is a new model for exploring the mechanisms of long-term supraspinal control over spinal cord function. Primates and rats can gradually increase (HRup conditioning mode) or decrease (HRdown conditioning mode) the H-reflex when reward is based on H-reflex amplitude. An earlier study indicated that HRdown conditioning of the soleus H-reflex in rats is impaired following contusion injury to thoracic spinal cord. The extent of impairment was correlated with the percent of white matter lost at the injury site. The present study investigated the effects of spinal cord injury on HRup conditioning. Soleus H-reflexes were elicited and recorded with chronically implanted electrodes from 14 rats that had been subjected to calibrated contusion injuries to the spinal cord at T8. At the lesion epicenter, 12-39% of the white matter remained. After control-mode data were collected, each rat was exposed to the HRup conditioning mode for 50 days. Final H-reflex amplitudes after HRup conditioning averaged 112% (+/-22% SD) of control. This value was significantly smaller than that for 13 normal rats exposed to HRup conditioning, in which final amplitude averaged 153% (+/-51%) SD of control. As previously reported for HRdown conditioning after spinal cord injury, success was inversely correlated with the severity of the injury as assessed by white matter preservation and by time to return of bladder function. HRup and HRdown conditioning are similarly sensitive to injury. These results further demonstrate that H-reflex conditioning is a sensitive measure of the long-term effects of injury on supraspinal control over spinal cord functions and could prove a valuable measure of therapeutic efficacy.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Herchenroder, P. A.</style></author><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Sag during unfused tetanic contractions in rat triceps surae motor units.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Regression Analysis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1999</style></year><pub-dates><date><style  face="normal" font="default" size="100%">06/1999</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/10368385</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">81</style></volume><pages><style face="normal" font="default" size="100%">2647–2661</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Contractile properties and conduction velocity were studied in 202 single motor units of intact rat triceps surae muscles activated by intra-axonal (or intra-myelin) current injection in L5 or L6 ventral root to assess the factors that determine the expression of sag (i.e., decline in force after initial increase during unfused tetanic stimulation). Sag was consistently detected in motor units with unpotentiated twitch contraction times &lt;20 ms. However, the range of frequencies at which sag was expressed varied among motor units such that there was no single interstimulus interval (ISI), with or without adjusting for twitch contraction time, at which sag could be detected reliably. Further analysis indicated that using the absence of sag as a criterion for identifying slow-twitch motor units requires testing with tetani at several different ISIs. In motor units with sag, the shape of the force profile varied with tetanic frequency and contractile properties. Simple sag force profiles (single maximum reached late in the tetanus followed by monotonic decay) tended to occur at shorter ISIs and were observed more frequently in fatigue-resistant motor units with long half-relaxation times and small twitch amplitudes. Complex sag profiles reached an initial maximum early in the tetanus, tended to occur at longer ISIs, and were more common in fatigue-sensitive motor units with long half-relaxation times and large twitch amplitudes. The differences in frequency dependence and force maximum location suggested that these phenomena represented discrete entities. Successive stimuli elicited near-linear increments in force during tetani in motor units that never exhibited sag. In motor units with at least one tetanus displaying sag, tetanic stimulation elicited large initial force increments followed by rapidly decreasing force increments. That the latter force envelope pattern occurred in these units even in tetani without sag suggested that the factors responsible for sag were expressed in the absence of overt sag. The time-to-peak force (TTP) of the individual contractions during a tetanus decreased in tetani with sag. Differences in the pattern of TTP change during a tetanus were consistent with the differences in force maximum location between tetani exhibiting simple and complex sag. Tetani from motor units that never exhibited sag did not display a net decrease in TTP during successive contractions. These data were consistent with the initial force decrement of sag resulting from a transient reduction in the duration of the contractile state.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Dorsal column but not lateral column transection prevents down-conditioning of H reflex in rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1997</style></year><pub-dates><date><style  face="normal" font="default" size="100%">09/1997</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/9310458</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">78</style></volume><pages><style face="normal" font="default" size="100%">1730–1734</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Operant conditioning of the H reflex, the electrical analogue of the spinal stretch reflex, in freely moving rats is a relatively simple model for studying long-term supraspinal control over spinal cord function. Motivated by food reward, rats can gradually increase or decrease the soleus H reflex. This study is the first effort to determine which spinal cord pathways convey the descending influence from supraspinal structures that changes the H reflex. In anesthetized Sprague-Dawley rats, the entire dorsal column (DC), which includes the main corticospinal tract, or the right lateral column (LC) was transected by electrocautery. Animals recovered quickly and the minimal transient effects of transection on the right soleus H reflex disappeared within 16 days. Beginning at least 18 days after transection, 12 rats were exposed to the HRdown-conditioning mode, in which reward was given when the H reflex of the right soleus muscle was below a criterion value. In seven LC rats exposed to the HRdown mode, the H reflex fell to 71 +/- 8% (mean +/- SE) of its initial value. In six of the seven, conditioning was successful (i.e., decrease to &lt; or = 80%). These results were comparable with those previously obtained from normal rats. In contrast, in five DC rats exposed to the HRdown mode, the H reflex at the end of exposure was 106 +/- 12% of its initial value. In none of these rats was HRdown-conditioning successful. DC rats differed significantly from normal and LC rats in both final H reflex values and number successful. In five DC and three LC rats that continued under control conditions over 30-78 days, the H reflex at the end of the period was 98 +/- 4% and 100 +/- 8%, respectively, of its initial value, indicating that DC or LC transection itself did not lead to gradual increase or decrease in the H reflex. The results indicate that the DC, containing the main corticospinal tract, is essential for HRdown-conditioning, whereas the ipsilateral LC, containing the main rubrospinal, vestibulospinal, and reticulospinal tracts, is not essential. Combined with the known muscular specificity of conditioning, these results suggest that the main corticospinal tract is essential for HRdown-conditioning. The DC ascending tract might also be necessary. The respective roles of the DC descending and ascending tracts, and transection effects on HRup-conditioning and on the maintenance of both HRup- and HRdown-conditioning after they have occurred, remain to be defined.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Jakeman, L. B.</style></author><author><style face="normal" font="default" size="100%">Stokes, B. T.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Operant conditioning of H-reflex in spinal cord-injured rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurotrauma</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">operant conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">rat</style></keyword><keyword><style  face="normal" font="default" size="100%">soleus muscle</style></keyword><keyword><style  face="normal" font="default" size="100%">spinal cord injury</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1996</style></year><pub-dates><date><style  face="normal" font="default" size="100%">12/1996</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/9002061</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">13</style></volume><pages><style face="normal" font="default" size="100%">755–766</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Operant conditioning of the spinal stretch reflex or its electrical analog, the H-reflex, is a new model for exploring the mechanisms of supraspinal control over spinal cord function. Both rats and primates can gradually increase (HRup conditioning mode) or decrease (HRdown conditioning mode) soleus H-reflex magnitude when exposed to an operant conditioning task. This study used H-reflex operant conditioning to assess and modify spinal cord function after injury. Soleus H-reflexes were elicited and recorded with chronically implanted electrodes from rats that had been subjected to calibrated contusion injuries to the spinal cord at T8. From 18 to 140 days after injury, background EMG, M response amplitude, and initial H-reflex amplitude were not significantly different from those of normal rats. HRdown conditioning was successful in some, but not all, spinal cord-injured rats. The H-reflex decrease achieved by conditioning was inversely correlated with the severity of the injury as assessed histologically or by time to return of bladder function. It was not correlated with the length of time between injury and the beginning of conditioning. The results confirm the importance of descending control from supraspinal structures in mediating operantly conditioned change in H-reflex amplitude. In conjunction with recent human studies, they suggest that H-reflex conditioning could provide a sensitive new means for assessing spinal cord function after injury, and might also provide a method for initiating and guiding functional rehabilitation.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Reversal of H-reflex operant conditioning in the rat.</style></title><secondary-title><style face="normal" font="default" size="100%">Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">operant conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">plasticity</style></keyword><keyword><style  face="normal" font="default" size="100%">rat</style></keyword><keyword><style  face="normal" font="default" size="100%">soleus muscle</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1996</style></year><pub-dates><date><style  face="normal" font="default" size="100%">11/1996</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/8951407</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">112</style></volume><pages><style face="normal" font="default" size="100%">58–62</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">In response to an operant conditioning task, rats can gradually increase or decrease soleus H-reflex amplitude without change in background electromyographic activity or M response amplitude. Both increase (under the HRup mode) and decrease (under the HRdown mode) develop over weeks. The present study investigated reversal of conditioned H-reflex change. Following collection of control data, rats were exposed to one mode (HRup or HRdown) for 50 days, and then exposed to the opposite mode for up to 72 days. Rats responded to each mode exposure with gradual, mode-appropriate change in H-reflex amplitude. This finding is consistent with other evidence that H-reflex conditioning depends on spinal cord plasticity. The effects of exposure to the HRup (or HRdown) mode were not affected by whether exposure followed previous exposure to the HRdown (or HRup) mode. In accord with recent studies suggesting that HRup and HRdown conditioning have different spinal mechanisms, these results suggest that reversal of H-reflex change is due primarily to the superimposition of additional plasticity rather than to decay of the plasticity responsible for the initial change.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Operant conditioning of H-reflex in freely moving rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1995</style></year><pub-dates><date><style  face="normal" font="default" size="100%">01/1995</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/7714584</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">73</style></volume><pages><style face="normal" font="default" size="100%">411–415</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">1. Primates can increase or decrease the spinal stretch reflex and its electrical analogue, the H-reflex (HR), in response to an operant conditioning task. This conditioning changes the spinal cord itself and thereby provides an experimental model for defining the processes and substrates of a learned change in behavior. Because the phenomenon has been demonstrated only in primates, its generality and theoretical implications remain unclear, and its experimental use is restricted by the difficulties of primate research. In response to these issues, the present study explored operant conditioning of the H-reflex in the rat. 2. Seventeen Sprague-Dawley rats implanted with chronic electromyographic (EMG) recording electrodes in one soleus muscle and nerve cuff stimulating electrodes on the posterior tibial nerve were rewarded (either with medial forebrain bundle stimulation or food) for increasing (HRup conditioning mode) or decreasing (HRdown conditioning mode) soleus H-reflex amplitude without change in background EMG or M response (direct muscle response) amplitude. 3. H-reflex amplitude changed appropriately over 3-4 wk. Under the HRup mode, it rose to an average of 158 +/- 54% (mean +/- SD) of initial value, whereas under the HRdown mode it fell to an average of 67 +/- 11% of initial value. Background EMG and M response amplitude did not change. 4. Operant conditioning of the H-reflex in the rat appears similar in rate and final magnitude of change to that observed in the monkey.(ABSTRACT TRUNCATED AT 250 WORDS)</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Operantly conditioned plasticity and circadian rhythm in rat H-reflex are independent phenomena.</style></title><secondary-title><style face="normal" font="default" size="100%">Neuroscience letters</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">circadian rhythm</style></keyword><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">Learning</style></keyword><keyword><style  face="normal" font="default" size="100%">Memory</style></keyword><keyword><style  face="normal" font="default" size="100%">operant conditioning</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1995</style></year><pub-dates><date><style  face="normal" font="default" size="100%">08/1995</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/7478262</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">195</style></volume><pages><style face="normal" font="default" size="100%">109–112</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Recent studies indicate that rats can increase or decrease H-reflex amplitude in response to an operant conditioning paradigm. In addition, rats also display a circadian rhythm in H-reflex amplitude. As part of the development of H-reflex conditioning in the rat as a new model for defining the plasticity underlying a simple form of learning, this study examined the relationship in the rat between operantly conditioned H-reflex change and the H-reflex circadian rhythm. When H-reflex amplitude increased or decreased in response to the operant conditioning program, its circadian rhythm showed no changes in phase and minimal change in amplitude. Furthermore, animals did not alter daily performance schedule so as to use the rhythm to increase reward probability. Thus, in the rat, H-reflex operant conditioning and the H-reflex circadian rhythm appear to be independent phenomena. The circadian rhythm should not be a significant complicating factor in studies of operantly conditioned H-reflex change.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Circadian rhythm in rat H-reflex.</style></title><secondary-title><style face="normal" font="default" size="100%">Brain research</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">circadian rhythm</style></keyword><keyword><style  face="normal" font="default" size="100%">electromyogram</style></keyword><keyword><style  face="normal" font="default" size="100%">H-Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">rat</style></keyword><keyword><style  face="normal" font="default" size="100%">soleus</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1994</style></year><pub-dates><date><style  face="normal" font="default" size="100%">06/1994</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/7922520</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">648</style></volume><pages><style face="normal" font="default" size="100%">167–170</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">We measured soleus H-reflex in the Sprague-Dawley rat as a function of time of day. H-reflex amplitude displayed a marked diurnal variation, even though background EMG and M-response amplitude were stable through the day. The H-reflex was largest in the late morning and smallest around midnight. Thus, its rhythm was opposite in phase to the circadian rhythm found in the primate H-reflex. This rhythm is a potentially confounding factor in studies of motor function. Furthermore, its existence implies that the CNS activity underlying a specific motor performance varies with time of day.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Triceps surae motoneuron morphology in the rat: a quantitative light microscopic study.</style></title><secondary-title><style face="normal" font="default" size="100%">The Journal of comparative neurology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">computer assisted</style></keyword><keyword><style  face="normal" font="default" size="100%">dendrites</style></keyword><keyword><style  face="normal" font="default" size="100%">horseradish peroxidase</style></keyword><keyword><style  face="normal" font="default" size="100%">image processing</style></keyword><keyword><style  face="normal" font="default" size="100%">Software</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1994</style></year><pub-dates><date><style  face="normal" font="default" size="100%">05/1994</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/8027432</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">343</style></volume><pages><style face="normal" font="default" size="100%">143–157</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The rat is now the model of choice for many studies of motor function. However, little quantitative information on the structure of rat motoneurons is available. In conjunction with efforts to define the physiologic and anatomic substrates of operantly conditioned plasticity in the spinal cord, 13 physiologically identified triceps surae motoneurons in the rat lumbar spinal cord were labeled intracellularly with horseradish peroxidase and completely reconstructed and measured with a computer-based neuron-tracing system. Somata were all located in the ventral horn of lumbar segments 4-5, had an average diameter of 35 microns, and had 6-12 dendrites. Dendrites ramified throughout the ventral horn and also penetrated the white matter. Their spread was greater in the rostrocaudal and dorsoventral directions (1.53 +/- 0.24 mm and 1.35 +/- 0.23 mm, respectively) than in the mediolateral direction (0.85 +/- 0.14 mm). Regardless of soma location, dendritic fields usually extended throughout the ipsilateral coronal cross-section of the ventral horn. As a result, the ventral or lateral extent of the field was correlated strongly with the soma's distance from the ventral or lateral border, respectively, of the ventral horn. Furthermore, although soma locations in the coronal plane varied widely, the centers of the dendritic fields tended to cluster near the center of the ventral horn. Dendrites constituted 96.2-98.4% (mean +/- SD = 97.3 +/- 0.7%) of the total neuronal surface area. Each of the 104 dendrites studied had an average of 13 branch points and 27 segments. First-order segment diameters ranged from 1.4 to 11.7 microns (mean +/- SD = 5.3 +/- 2.1 microns). Total dendritic length, surface area, volume, number of dendritic segments, and maximum segment order were correlated strongly with diameter of the first-order segment. Proceeding distally between branch points, the mean decrease in dendritic diameter (i.e., tapering) +/- the standard deviation was 22 +/- 8% of the proximal diameter. The average ratio +/- the standard deviation of the sum of the average diameters of each daughter segment raised to the 1.5 power to the average diameter of the parent segment raised to the 1.5 power (i.e., Rall's ratio; Rall, 1959) was 0.87 +/- 0.08. In comparison with cat alpha-motoneurons, rat motoneurons had smaller soma diameters, fewer dendrites, smaller total surface areas, and shorter total dendritic lengths. However, the number of terminations per dendrite was similar in the two species, so that rat motoneurons had more terminations per unit dendritic length.(ABSTRACT TRUNCATED AT 400 WORDS)</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Constancy of motor axon conduction time during growth in rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">development</style></keyword><keyword><style  face="normal" font="default" size="100%">motoneuron</style></keyword><keyword><style  face="normal" font="default" size="100%">motor axon</style></keyword><keyword><style  face="normal" font="default" size="100%">nerve conduction</style></keyword><keyword><style  face="normal" font="default" size="100%">rat</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1992</style></year><pub-dates><date><style  face="normal" font="default" size="100%">08/1992</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/1397148</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">90</style></volume><pages><style face="normal" font="default" size="100%">343–345</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Axon conduction distance, conduction velocity, and conduction time were measured for individual triceps surae motoneurons in Sprague-Dawley rats weighing 230-630 g (i.e., age range 6-16 weeks). Both conduction distance (nerve length) and velocity were closely correlated with weight (r = 0.95 and r = 0.82, respectively). In contrast, conduction time did not change as weight increased nearly threefold. This striking constancy is probably due to a corresponding increase in axon diameter. It could contribute to maintenance of stable motor performance during rapid growth.</style></abstract></record></records></xml>