01650nas a2200205   4500008004100000022001400041245008000055210006900135260000800204300001600212490000800228520106300236653001601299100002101315700001301336700001301349700001301362700002101375856004801396       2016                        eng d  a1522-159800aAblation of the inferior olive prevents H-reflex down-conditioning in rats.0 aAblation of the inferior olive prevents Hreflex downconditioning  cMar  a1630–16360 v1153 aWe evaluated the role of the inferior olive (IO) in acquisition of the spinal cord plasticity that underlies H-reflex down-conditioning, a simple motor skill. The IO was chemically ablated before a 50-day exposure to an operant conditioning protocol that rewarded a smaller soleus H-reflex. In normal rats, down-conditioning succeeds (i.e., H-reflex size decreases at least 20%) in 80% of animals. Down-conditioning failed in every IO-ablated rat (P< 0.001 vs. normal rats). IO ablation itself had no long-term effect on H-reflex size. These results indicate that the IO is essential for acquisition of a down-conditioned H-reflex. With previous data, they support the hypothesis that IO and cortical inputs to cerebellum enable the cerebellum to guide sensorimotor cortex plasticity that produces and maintains the spinal cord plasticity that underlies the down-conditioned H-reflex. They help to further define H-reflex conditioning as a model for understanding motor learning and as a new approach to enhancing functional recovery after trauma or disease.10aSpinal Cord1 aChen, Xiang Yang1 aWang, Yu1 aChen, Yi1 aChen, Lu1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/2679288801486nas a2200205   4500008004100000022001400041245010200055210006900157260001200226300001600238490000800254520087300262653001601135100001301151700001301164700001301177700002101190700002101211856004801232       2012                        eng d  a1522-159800aCortical stimulation causes long-term changes in H-reflexes and spinal motoneuron GABA receptors.0 aCortical stimulation causes longterm changes in Hreflexes and sp  c11/2012  a2668–26780 v1083 aThe cortex gradually modifies the spinal cord during development, throughout later life, and in response to trauma or disease. The mechanisms of this essential function are not well understood. In this study, weak electrical stimulation of rat sensorimotor cortex increased the soleus H-reflex, increased the numbers and sizes of GABAergic spinal interneurons and GABAergic terminals on soleus motoneurons, and decreased GABA(A) and GABA(B) receptor labeling in these motoneurons. Several months after the stimulation ended the interneuron and terminal increases had disappeared, but the H-reflex increase and the receptor decreases remained. The changes in GABAergic terminals and GABA(B) receptors accurately predicted the changes in H-reflex size. The results reveal a new long-term dimension to cortical-spinal interactions and raise new therapeutic possibilities.10aSpinal Cord1 aWang, Yu1 aChen, Yi1 aChen, Lu1 aWolpaw, Jonathan1 aChen, Xiang Yang  uhttp://www.ncbi.nlm.nih.gov/pubmed/2293371802599nas 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/21123559