02599nas a2200289   4500008004100000022001400041245013200055210006900187260001200256300001800268490000700286520174900293653001702042653002102059653001502080653001102095653001702106653001602123100001302139700001302152700001302165700001702178700002402195700002102219700002102240856004802261       2010                        eng d  a1529-240100aH-reflex up-conditioning encourages recovery of EMG activity and H-reflexes after sciatic nerve transection and repair in rats.0 aHreflex upconditioning encourages recovery of EMG activity and H  c12/2010  a16128–161360 v303 aOperant 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.10aconditioning10aperipheral nerve10aplasticity10aReflex10aregeneration10aSpinal Cord1 aChen, Yi1 aWang, Yu1 aChen, Lu1 aSun, Chenyou1 aEnglish, Arthur, W.1 aWolpaw, Jonathan1 aChen, Xiang Yang  uhttp://www.ncbi.nlm.nih.gov/pubmed/2112355901519nas a2200301   4500008004100000022001400041245009500055210006900150260001200219300001400231490001700245520064100262653001300903653002400916653001500940653001500955653002400970653001900994653002301013100002101036700001301057700001301070700001901083700002301102700002301125700002101148856004801169       2010                        eng d  a1749-663200aReflex conditioning: a new strategy for improving motor function after spinal cord injury.0 aReflex conditioning a new strategy for improving motor function   c06/2010  aE12–E210 v1198 Suppl 13 aSpinal 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.10aH-Reflex10alearning and memory10aLocomotion10aplasticity10areflex conditioning10aRehabilitation10aspinal cord injury1 aChen, Xiang Yang1 aChen, Yi1 aWang, Yu1 aThompson, Aiko1 aCarp, Jonathan, S.1 aSegal, Richard, L.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/2059053402272nas 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/17115915