<?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%">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%">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%">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%">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%">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%">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>