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