02131nas a2200253   4500008004100000245007200041210006900113260000900182300001400191490000700205520141800212653001301630653001901643653002501662653001501687653001901702653001601721100001301737700001301750700001301763700002201776700002101798856005801819       2017                        eng d00aWhy New Spinal Cord Plasticity Does Not Disrupt Old Motor Behaviors0 aWhy New Spinal Cord Plasticity Does Not Disrupt Old Motor Behavi  cJuly  a8198-82060 v373 aWhen new motor learning changes the spinal cord, old behaviors are not impaired; their key features are preserved by additional compensatory plasticity. To explore the mechanisms responsible for this compensatory plasticity, we transected the spinal dorsal ascending tract before or after female rats acquired a new behavior—operantly conditioned increase or decrease in the right soleus H-reflex—and examined an old behavior—locomotion. Neither spinal dorsal ascending tract transection nor H-reflex conditioning alone impaired locomotion. Nevertheless, when spinal dorsal ascending tract transection and H-reflex conditioning were combined, the rats developed a limp and a tilted posture that correlated in direction and magnitude with the H-reflex change. When the right H-reflex was increased by conditioning, the right step lasted longer than the left and the right hip was higher than the left; when the right H-reflex was decreased by conditioning, the opposite occurred. These results indicate that ascending sensory input guides the compensatory plasticity that normally prevents the plasticity underlying H-reflex change from impairing locomotion. They support the concept of the state of the spinal cord as a negotiated equilibrium that reflects the concurrent influences of all the behaviors in an individual's repertoire; and they support the new therapeutic strategies this concept introduces.10aH-Reflex10amotor learning10aoperant conditioning10aplasticity10aRehabilitation10aSpinal Cord1 aChen, Yi1 aChen, Lu1 aWang, Yu1 aChen, Xiang, Yang1 aWolpaw, Jonathan  uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5566867/01650nas 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/26792888