02425nas a2200289   4500008004100000022001400041245008700055210006900142260001200211300001200223490000800235520161100243653002601854653001301880653001501893653001101908653001801919653001901937653002301956653002701979100001302006700001302019700001302032700002102045700002102066856004802087       2014                        eng d  a1522-159800aPersistent beneficial impact of H-reflex conditioning in spinal cord-injured rats.0 aPersistent beneficial impact of Hreflex conditioning in spinal c  c11/2014  a2374-810 v1123 a<p>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.</p>10aH-reflex conditioning10aLearning10aLocomotion10aMemory10aMotor control10aRehabilitation10aspinal cord injury10aspinal cord plasticity1 aChen, Yi1 aChen, Lu1 aWang, Yu1 aWolpaw, Jonathan1 aChen, Xiang Yang  uhttp://www.ncbi.nlm.nih.gov/pubmed/2514354201505nas a2200253   4500008004100000022001400041245012000055210006900175260001200244300001400256490000800270520070300278653003400981653002701015653002601042653002401068653001801092653001601110100001301126700002201139700002101161700002101182856004801203       2009                        eng d  a0304-394000aH-reflex down-conditioning greatly increases the number of identifiable GABAergic interneurons in rat ventral horn.0 aHreflex downconditioning greatly increases the number of identif  c03/2009  a124–1290 v4523 aH-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.10aactivity-dependent plasticity10aGABAergic interneurons10aH-reflex conditioning10alearning and memory10aMotor control10aSpinal Cord1 aWang, Yu1 aPillai, Shreejith1 aWolpaw, Jonathan1 aChen, Xiang Yang  uhttp://www.ncbi.nlm.nih.gov/pubmed/1938342602272nas a2200253   4500008004100000022001400041245009400055210006900149260001200218300001600230490000700246520153000253653002401783653002601807653001501833653000801848653002301856100002101879700001301900700001301913700002301926700002101949856004801970       2006                        eng d  a0897-715100aCorticospinal tract transection permanently abolishes H-reflex down-conditioning in rats.0 aCorticospinal tract transection permanently abolishes Hreflex do  c11/2006  a1705–17120 v233 aPrevious 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.10acorticospinal tract10aH-reflex conditioning10aplasticity10arat10aspinal cord injury1 aChen, Xiang Yang1 aChen, Yi1 aChen, Lu1 aTennissen, Ann, M.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1711591501903nas a2200301   4500008004100000022001400041245010700055210006900162260001200231300001800243490000700261520101900268653002601287653001301313653001501326653001101341653001801352653001901370653002301389653002701412100001301439700002101452700002101473700001301494700002501507700002101532856004801553       2006                        eng d  a1529-240100aOperant conditioning of H-reflex can correct a locomotor abnormality after spinal cord injury in rats.0 aOperant conditioning of Hreflex can correct a locomotor abnormal  c11/2006  a12537–125430 v263 a<p>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.</p>10aH-reflex conditioning10aLearning10aLocomotion10aMemory10aMotor control10aRehabilitation10aspinal cord injury10aspinal cord plasticity1 aChen, Yi1 aChen, Xiang Yang1 aJakeman, Lyn, B.1 aChen, Lu1 aStokes, Bradford, T.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1713541502708nas a2200289   4500008004100000022001400041245010300055210006900158260001200227300001600239490000700255520184500262653002602107653001302133653001502146653002502161653001802186653001902204653002702223100001302250700002102263700002102284700001902305700002502324700002102349856004802370       2005                        eng d  a1529-240100aThe interaction of a new motor skill and an old one: H-reflex conditioning and locomotion in rats.0 ainteraction of a new motor skill and an old one Hreflex conditio  c07/2005  a6898–69060 v253 aNew 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.10aH-reflex conditioning10aLearning10aLocomotion10amemory consolidation10aMotor control10aRehabilitation10aspinal cord plasticity1 aChen, Yi1 aChen, Xiang Yang1 aJakeman, Lyn, B.1 aSchalk, Gerwin1 aStokes, Bradford, T.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/16033899