<?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%">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%">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></records></xml>