03907nas a2200361   4500008004100000022001400041245007800055210006900133260001300202300001400215490000800229520287700237653001203114653001303126653002503139653001003164653002603174653001303200653001303213653000903226653001803235653002403253653000903277653002503286653001603311100001303327700001303340700001303353700002103366700002203387700002403409856011203433       2024                        eng d  a1469-779300aMotor learning changes the axon initial segment of the spinal motoneuron.0 aMotor learning changes the axon initial segment of the spinal mo  c2024 May  a2107-21260 v6023 a<p>We are studying the mechanisms of H-reflex operant conditioning, a simple form of learning. Modelling studies in the literature and our previous data suggested that changes in the axon initial segment (AIS) might contribute. To explore this, we used blinded quantitative histological and immunohistochemical methods to study in adult rats the impact of H-reflex conditioning on the AIS of the spinal motoneuron that produces the reflex. Successful, but not unsuccessful, H-reflex up-conditioning was associated with greater AIS length and distance from soma; greater length correlated with greater H-reflex increase. Modelling studies in the literature suggest that these increases may increase motoneuron excitability, supporting the hypothesis that they may contribute to H-reflex increase. Up-conditioning did not affect AIS ankyrin G (AnkG) immunoreactivity (IR), p-p38 protein kinase IR, or GABAergic terminals. Successful, but not unsuccessful, H-reflex down-conditioning was associated with more GABAergic terminals on the AIS, weaker AnkG-IR, and stronger p-p38-IR. More GABAergic terminals and weaker AnkG-IR correlated with greater H-reflex decrease. These changes might potentially contribute to the positive shift in motoneuron firing threshold underlying H-reflex decrease; they are consistent with modelling suggesting that sodium channel change may be responsible. H-reflex down-conditioning did not affect AIS dimensions. This evidence that AIS plasticity is associated with and might contribute to H-reflex conditioning adds to evidence that motor learning involves both spinal and brain plasticity, and both neuronal and synaptic plasticity. AIS properties of spinal motoneurons are likely to reflect the combined influence of all the motor skills that share these motoneurons. KEY POINTS: Neuronal action potentials normally begin in the axon initial segment (AIS). AIS plasticity affects neuronal excitability in development and disease. Whether it does so in learning is unknown. Operant conditioning of a spinal reflex, a simple learning model, changes the rat spinal motoneuron AIS. Successful, but not unsuccessful, H-reflex up-conditioning is associated with greater AIS length and distance from soma. Successful, but not unsuccessful, down-conditioning is associated with more AIS GABAergic terminals, less ankyrin G, and more p-p38 protein kinase. The associations between AIS plasticity and successful H-reflex conditioning are consistent with those between AIS plasticity and functional changes in development and disease, and with those predicted by modelling studies in the literature. Motor learning changes neurons and synapses in spinal cord and brain. Because spinal motoneurons are the final common pathway for behaviour, their AIS properties probably reflect the combined impact of all the behaviours that use these motoneurons.</p>10aAnimals10aAnkyrins10aAxon Initial Segment10aAxons10aConditioning, Operant10aH-Reflex10aLearning10aMale10aMotor Neurons10aNeuronal Plasticity10aRats10aRats, Sprague-Dawley10aSpinal Cord1 aWang, Yu1 aChen, Yi1 aChen, Lu1 aHerron, Bruce, J1 aChen, Xiang, Yang1 aWolpaw, Jonathan, R  uhttps://neurotechcenter.org/publications/2024/motor-learning-changes-axon-initial-segment-spinal-motoneuron02131nas 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/PMC5566867/02675nas a2200325   4500008004100000022001400041245010000055210006900155260001200224300001200236490000800248520178700256653001202043653002602055653001102081653001302092653001302105653001502118653000902133653000902142653002502151653002502176100001302201700001302214700001902227700001302246700002102259700002102280856004802301       2014                        eng d  a1522-159800aLocomotor impact of beneficial or nonbeneficial H-reflex conditioning after spinal cord injury.0 aLocomotor impact of beneficial or nonbeneficial Hreflex conditio  c03/2014  a1249-580 v1113 aWhen new motor learning changes neurons and synapses in the spinal cord, it may affect previously learned behaviors that depend on the same spinal neurons and synapses. To explore these effects, we used operant conditioning to strengthen or weaken the right soleus H-reflex pathway in rats in which a right spinal cord contusion had impaired locomotion. When up-conditioning increased the H-reflex, locomotion improved. Steps became longer, and step-cycle asymmetry (i.e., limping) disappeared. In contrast, when down-conditioning decreased the H-reflex, locomotion did not worsen. Steps did not become shorter, and asymmetry did not increase. Electromyographic and kinematic analyses explained how H-reflex increase improved locomotion and why H-reflex decrease did not further impair it. Although the impact of up-conditioning or down-conditioning on the H-reflex pathway was still present during locomotion, only up-conditioning affected the soleus locomotor burst. Additionally, compensatory plasticity apparently prevented the weaker H-reflex pathway caused by down-conditioning from weakening the locomotor burst and further impairing locomotion. The results support the hypothesis that the state of the spinal cord is a "negotiated equilibrium" that serves all the behaviors that depend on it. When new learning changes the spinal cord, old behaviors undergo concurrent relearning that preserves or improves their key features. Thus, if an old behavior has been impaired by trauma or disease, spinal reflex conditioning, by changing a specific pathway and triggering a new negotiation, may enable recovery beyond that achieved simply by practicing the old behavior. Spinal reflex conditioning protocols might complement other neurorehabilitation methods and enhance recovery.10aAnimals10aConditioning, Operant10aFemale10aH-Reflex10aLearning10aLocomotion10aMale10aRats10aRats, Sprague-Dawley10aSpinal Cord Injuries1 aChen, Yi1 aChen, Lu1 aLiu, Rongliang1 aWang, Yu1 aChen, Xiang Yang1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/2437128801519nas 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/2059053402175nas a2200253   4500008004100000022001400041245008500055210006900140260001200209300001400221490000700235520145300242653003401695653000901729653001301738653001101751653001801762653001601780100001301796700002201809700002101831700002101852856004801873       2006                        eng d  a0953-816X00aMotor learning changes GABAergic terminals on spinal motoneurons in normal rats.0 aMotor learning changes GABAergic terminals on spinal motoneurons  c01/2006  a141–1500 v233 aThe role of spinal cord plasticity in motor learning is largely unknown. This study explored the effects of H-reflex operant conditioning, a simple model of motor learning, on GABAergic input to spinal motoneurons in rats. Soleus motoneurons were labeled by retrograde transport of a fluorescent tracer and GABAergic terminals on them were identified by glutamic acid decarboxylase (GAD)67 immunoreactivity. Three groups were studied: (i) rats in which down-conditioning had reduced the H-reflex (successful HRdown rats); (ii) rats in which down-conditioning had not reduced the H-reflex (unsuccessful HRdown rats) and (iii) unconditioned (naive) rats. The number, size and GAD density of GABAergic terminals, and their coverage of the motoneuron, were significantly greater in successful HRdown rats than in unsuccessful HRdown or naive rats. It is likely that these differences are due to modifications in terminals from spinal interneurons in lamina VI-VII and that the increased terminal number, size, GAD density and coverage in successful HRdown rats reflect and convey a corticospinal tract influence that changes motoneuron firing threshold and thereby decreases the H-reflex. GABAergic terminals in spinal cord change after spinal cord transection. The present results demonstrate that such spinal cord plasticity also occurs in intact rats in the course of motor learning and suggest that this plasticity contributes to skill acquisition.10aactivity-dependent plasticity10aGABA10aH-Reflex10aMemory10aMotor control10aSpinal Cord1 aWang, Yu1 aPillai, Shreejith1 aWolpaw, Jonathan1 aChen, Xiang Yang  uhttp://www.ncbi.nlm.nih.gov/pubmed/16420424