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-motoneuron02149nas a2200313   4500008004100000022001400041245009400055210006900149260001600218300001100234490000700245520118200252653001301434653002301447653001601470653001101486653001301497653003201510653002801542100001601570700001601586700001901602700001901621700001201640700002201652700002701674700001501701856011901716       2024                        eng d  a2211-124700aNeural mechanisms of face familiarity and learning in the human amygdala and hippocampus.0 aNeural mechanisms of face familiarity and learning in the human   c2024 Jan 23  a1135200 v433 a<p>Recognizing familiar faces and learning new faces play an important role in social cognition. However, the underlying neural computational mechanisms remain unclear. Here, we record from single neurons in the human amygdala and hippocampus and find a greater neuronal representational distance between pairs of familiar faces than unfamiliar faces, suggesting that neural representations for familiar faces are more distinct. Representational distance increases with exposures to the same identity, suggesting that neural face representations are sharpened with learning and familiarization. Furthermore, representational distance is positively correlated with visual dissimilarity between faces, and exposure to visually similar faces increases representational distance, thus sharpening neural representations. Finally, we construct a computational model that demonstrates an increase in the representational distance of artificial units with training. Together, our results suggest that the neuronal population geometry, quantified by the representational distance, encodes face familiarity, similarity, and learning, forming the basis of face recognition and memory.</p>10aAmygdala10aFacial Recognition10aHippocampus10aHumans10aLearning10aPattern Recognition, Visual10aRecognition, Psychology1 aCao, Runnan1 aWang, Jinge1 aBrunner, Peter1 aWillie, Jon, T1 aLi, Xin1 aRutishauser, Ueli1 aBrandmeir, Nicholas, J1 aWang, Shuo  uhttps://neurotechcenter.org/publications/2024/neural-mechanisms-face-familiarity-and-learning-human-amygdala-and-002092nas a2200217   4500008004100000022001400041245009800055210006900153260001200222300001100234490000700245520143300252653001301685653001501698653002301713653002701736653002001763100002201783700002101805856004801826       2015                        eng d  a1089-409800aRestoring walking after spinal cord injury: operant conditioning of spinal reflexes can help.0 aRestoring walking after spinal cord injury operant conditioning   c04/2015  a203-150 v213 a<p>People with incomplete spinal cord injury (SCI) frequently suffer motor disabilities due to spasticity and poor muscle control, even after conventional therapy. Abnormal spinal reflex activity often contributes to these problems. Operant conditioning of spinal reflexes, which can target plasticity to specific reflex pathways, can enhance recovery. In rats in which a right lateral column lesion had weakened right stance and produced an asymmetrical gait, up-conditioning of the right soleus H-reflex, which increased muscle spindle afferent excitation of soleus, strengthened right stance and eliminated the asymmetry. In people with hyperreflexia due to incomplete SCI, down-conditioning of the soleus H-reflex improved walking speed and symmetry. Furthermore, modulation of electromyographic activity during walking improved bilaterally, indicating that a protocol that targets plasticity to a specific pathway can trigger widespread plasticity that improves recovery far beyond that attributable to the change in the targeted pathway. These improvements were apparent to people in their daily lives. They reported walking faster and farther, and noted less spasticity and better balance. Operant conditioning protocols could be developed to modify other spinal reflexes or corticospinal connections; and could be combined with other therapies to enhance recovery in people with SCI or other neuromuscular disorders.</p>10aLearning10aLocomotion10aspinal cord injury10aspinal cord plasticity10aspinal reflexes1 aThompson, Aiko, K1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/2463695402675nas 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/2437128802554nas a2200241   4500008004100000022001400041245016400055210006900219260001200288300001200300490000800312520178000320653001302100653001502113653001902128653001602147653001502163100002102178700002202199700002102221700002202242856004802264       2014                        eng d  a1522-159800aOperant conditioning of the soleus H-reflex does not induce long-term changes in the gastrocnemius H-reflexes and does not disturb normal locomotion in humans.0 aOperant conditioning of the soleus Hreflex does not induce longt  c09/2014  a1439-460 v1123 a<p>In normal animals, operant conditioning of the spinal stretch reflex or the H-reflex has lesser effects on synergist muscle reflexes. In rats and people with incomplete spinal cord injury (SCI), soleus H-reflex operant conditioning can improve locomotion. We studied in normal humans the impact of soleus H-reflex down-conditioning on medial (MG) and lateral gastrocnemius (LG) H-reflexes and on locomotion. Subjects completed 6 baseline and 30 conditioning sessions. During conditioning trials, the subject was encouraged to decrease soleus H-reflex size with the aid of visual feedback. Every sixth session, MG and LG H-reflexes were measured. Locomotion was assessed before and after conditioning. In successfully conditioned subjects, the soleus H-reflex decreased 27.2%. This was the sum of within-session (task dependent) adaptation (13.2%) and across-session (long term) change (14%). The MG H-reflex decreased 14.5%, due mainly to task-dependent adaptation (13.4%). The LG H-reflex showed no task-dependent adaptation or long-term change. No consistent changes were detected across subjects in locomotor H-reflexes, EMG activity, joint angles, or step symmetry. Thus, in normal humans, soleus H-reflex down-conditioning does not induce long-term changes in MG/LG H-reflexes and does not change locomotion. In these subjects, task-dependent adaptation of the soleus H-reflex is greater than it is in people with SCI, whereas long-term change is less. This difference from results in people with SCI is consistent with the fact that long-term change is beneficial in people with SCI, since it improves locomotion. In contrast, in normal subjects, long-term change is not beneficial and may necessitate compensatory plasticity to preserve satisfactory locomotion.</p>10aLearning10aplasticity10aRehabilitation10aSpinal Cord10asynergists1 aMakihara, Yukiko1 aSegal, Richard, L1 aWolpaw, Jonathan1 aThompson, Aiko, K  uhttp://www.ncbi.nlm.nih.gov/pubmed/2494421602425nas a2200289   4500008004100000022001400041245008700055210006900142260001200211300001200223490000800235520161100243653002601854653001301880653001501893653001101908653001801919653001901937653002301956653002701979100001302006700001302019700001302032700002102045700002102066856004802087       2014                        eng d  a1522-159800aPersistent beneficial impact of H-reflex conditioning in spinal cord-injured rats.0 aPersistent beneficial impact of Hreflex conditioning in spinal c  c11/2014  a2374-810 v1123 a<p>Operant conditioning of a spinal cord reflex can improve locomotion in rats and humans with incomplete spinal cord injury. This study examined the persistence of its beneficial effects. In rats in which a right lateral column contusion injury had produced asymmetric locomotion, up-conditioning of the right soleus H-reflex eliminated the asymmetry while down-conditioning had no effect. After the 50-day conditioning period ended, the H-reflex was monitored for 100 [±9 (SD)] (range 79-108) more days and locomotion was then reevaluated. After conditioning ended in up-conditioned rats, the H-reflex continued to increase, and locomotion continued to improve. In down-conditioned rats, the H-reflex decrease gradually disappeared after conditioning ended, and locomotion at the end of data collection remained as impaired as it had been before and immediately after down-conditioning. The persistence (and further progression) of H-reflex increase but not H-reflex decrease in these spinal cord-injured rats is consistent with the fact that up-conditioning improved their locomotion while down-conditioning did not. That is, even after up-conditioning ended, the up-conditioned H-reflex pathway remained adaptive because it improved locomotion. The persistence and further enhancement of the locomotor improvement indicates that spinal reflex conditioning protocols might supplement current therapies and enhance neurorehabilitation. They may be especially useful when significant spinal cord regeneration becomes possible and precise methods for retraining the regenerated spinal cord are needed.</p>10aH-reflex conditioning10aLearning10aLocomotion10aMemory10aMotor control10aRehabilitation10aspinal cord injury10aspinal cord plasticity1 aChen, Yi1 aChen, Lu1 aWang, Yu1 aWolpaw, Jonathan1 aChen, Xiang Yang  uhttp://www.ncbi.nlm.nih.gov/pubmed/2514354202449nas a2200241   4500008004100000022001400041245010300055210006900158260001200227300001600239490000700255520172600262653001301988653001502001653002502016653001502041653001902056653001502075100002302090700002502113700002102138856004802159       2013                        eng d  a1529-240100aOperant conditioning of a spinal reflex can improve locomotion after spinal cord injury in humans.0 aOperant conditioning of a spinal reflex can improve locomotion a  c02/2013  a2365–23750 v333 aOperant conditioning protocols can modify the activity of specific spinal cord pathways and can thereby affect behaviors that use these pathways. To explore the therapeutic application of these protocols, we studied the impact of down-conditioning the soleus H-reflex in people with impaired locomotion caused by chronic incomplete spinal cord injury. After a baseline period in which soleus H-reflex size was measured and locomotion was assessed, subjects completed either 30 H-reflex down-conditioning sessions (DC subjects) or 30 sessions in which the H-reflex was simply measured [unconditioned (UC) subjects], and locomotion was reassessed. Over the 30 sessions, the soleus H-reflex decreased in two-thirds of the DC subjects (a success rate similar to that in normal subjects) and remained smaller several months later. In these subjects, locomotion became faster and more symmetrical, and the modulation of EMG activity across the step cycle increased bilaterally. Furthermore, beginning about halfway through the conditioning sessions, all of these subjects commented spontaneously that they were walking faster and farther in their daily lives, and several noted less clonus, easier stepping, and/or other improvements. The H-reflex did not decrease in the other DC subjects or in any of the UC subjects; and their locomotion did not improve. These results suggest that reflex-conditioning protocols can enhance recovery of function after incomplete spinal cord injuries and possibly in other disorders as well. Because they are able to target specific spinal pathways, these protocols could be designed to address each individual's particular deficits, and might thereby complement other rehabilitation methods.10aLearning10aLocomotion10aoperant conditioning10aplasticity10aRehabilitation10aspasticity1 aThompson, Aiko, K.1 aPomerantz, Ferne, R.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/2339266602704nas a2200241   4500008004100000022001400041245009000055210006900145260001200214300001400226490000700240520199800247653003402245653001302279653001102292653001802303653001602321100002202337700001302359700002102372700002102393856004802414       2008                        eng d  a1460-956800aEffects of H-reflex up-conditioning on GABAergic terminals on rat soleus motoneurons.0 aEffects of Hreflex upconditioning on GABAergic terminals on rat   c08/2008  a668–6740 v283 aTo explore the role of spinal cord plasticity in motor learning, we evaluated the effects of H-reflex operant conditioning on GABAergic input to rat spinal motoneurons. Previous work indicated that down-conditioning of soleus H-reflex increases GABAergic input to soleus motoneurons. This study explored the effect of H-reflex up-conditioning on GABAergic input. Of nine rats exposed to H-reflex up-conditioning, up-conditioning was successful (H-reflex increase >or= 20%) in seven and failed (change < 20%) in two. These rats and eight naive control (i.e. unconditioned) rats were injected with cholera toxin subunit B-conjugated Alexa fluor 488 into the soleus muscle to retrogradely label soleus motoneurons. Sections containing soleus motoneurons were processed for GAD(67) [one of the two principal forms of the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD)] with an ABC-peroxidase system. Two blinded independent raters counted and measured GABAergic terminals on these motoneurons. Unlike successful down-conditioning, which greatly increased the number of identifiable GABAergic terminals on the motoneurons, up-conditioning did not significantly change GABAergic terminal number. Successful up-conditioning did produce slight but statistically significant increases in GABAergic terminal diameter and soma coverage. These results are consistent with other data indicating that up- and down-conditioning are not mirror images of each other, but rather have different mechanisms. Although the marked changes in GABAergic terminals with down-conditioning probably contribute to H-reflex decrease, the modest changes in GABAergic terminals associated with up-conditioning may be compensatory or reactive plasticity, rather than the plasticity responsible for H-reflex increase. As a variety of spinal and supraspinal GABAergic neurons innervate motoneurons, the changes found with up-conditioning may be in terminals other than those affected in successful down-conditioning.10aactivity-dependent plasticity10aLearning10aMemory10aMotor control10aSpinal Cord1 aPillai, Shreejith1 aWang, Yu1 aWolpaw, Jonathan1 aChen, Xiang Yang  uhttp://www.ncbi.nlm.nih.gov/pubmed/1865718404251nas a2200505   4500008004100000022001400041245009900055210006900154260001200223300001200235490000700247520283600254653003103090653001503121653001003136653001003146653001003156653002703166653002903193653001103222653001103233653001303244653000903257653001603266653001703282653003303299653001903332653002803351653001303379653002203392653001303414653004303427653002803470653001303498100001603511700002203527700001803549700002103567700001903588700002103607700002203628700002703650700002003677856004803697       2008                        eng d  a0361-923000aNon-invasive brain-computer interface system: towards its application as assistive technology.0 aNoninvasive braincomputer interface system towards its applicati  c04/2008  a796-8030 v753 a<p><span style="font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;">The quality of life of people suffering from severe motor disabilities can benefit from the use of current assistive technology capable of ameliorating communication, house-environment management and mobility, according to the user's residual motor abilities.&nbsp;</span><span class="highlight" style="font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;">Brain-computer interfaces</span><span style="font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;">&nbsp;(BCIs) are systems that can translate&nbsp;</span><span class="highlight" style="font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;">brain</span><span style="font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;">&nbsp;activity into signals that control external devices. Thus they can represent the only technology for severely paralyzed patients to increase or maintain their communication and control options. Here we report on a pilot study in which a system was implemented and validated to allow disabled persons to improve or recover their mobility (directly or by emulation) and communication within the surrounding environment. The system is based on a software controller that offers to the user a communication interface that is matched with the individual's residual motor abilities. Patients (n=14) with severe motor disabilities due to progressive neurodegenerative disorders were trained to use the system prototype under a rehabilitation program carried out in a house-like furnished space. All users utilized regular assistive control options (e.g., microswitches or head trackers). In addition, four subjects learned to operate the system by means of a non-invasive EEG-based BCI. This system was controlled by the subjects' voluntary modulations of EEG sensorimotor rhythms recorded on the scalp; this skill was learnt even though the subjects have not had control over their limbs for a long time. We conclude that such a prototype system, which integrates several different assistive technologies including a BCI system, can potentially facilitate the translation from pre-</span><span class="highlight" style="font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;">clinical</span><span style="font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;">&nbsp;demonstrations to a&nbsp;</span><span class="highlight" style="font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;">clinical</span><span style="font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;">&nbsp;useful BCI.</span></p>10aActivities of Daily Living10aAdolescent10aAdult10aBrain10aChild10aElectroencephalography10aEvoked Potentials, Motor10aFemale10aHumans10aLearning10aMale10aMiddle Aged10aMotor Skills10aMuscular Dystrophy, Duchenne10aPilot Projects10aProstheses and Implants10aRobotics10aSelf-Help Devices10aSoftware10aSpinal Muscular Atrophies of Childhood10aUser-Computer Interface10aVolition1 aCincotti, F1 aMattia, Donatella1 aAloise, Fabio1 aBufalari, Simona1 aSchalk, Gerwin1 aOriolo, Giuseppe1 aCherubini, Andrea1 aMarciani, Maria Grazia1 aBabiloni, Fabio  uhttp://www.ncbi.nlm.nih.gov/pubmed/1839452602003nas a2200241   4500008004100000022001400041245007500055210006900130260001200199300001400211490000800225520132900233653001701562653001301579653001301592653001101605653001901616653001501635653001901650653002301669100002101692856004801713       2007                        eng d  a1748-170800aSpinal cord plasticity in acquisition and maintenance of motor skills.0 aSpinal cord plasticity in acquisition and maintenance of motor s  c02/2007  a155–1690 v1893 aThroughout normal life, activity-dependent plasticity occurs in the spinal cord as well as in brain. Like other central nervous system (CNS) plasticity, spinal cord plasticity can occur at numerous neuronal and synaptic sites and through a variety of mechanisms. Spinal cord plasticity is prominent early in life and contributes to mastery of standard behaviours like locomotion and rapid withdrawal from pain. Later in life, spinal cord plasticity has a role in acquisition and maintenance of new motor skills, and in compensation for peripheral and central changes accompanying ageing, disease and trauma. Mastery of the simplest behaviours is accompanied by complex spinal and supraspinal plasticity. This complexity is necessary, in order to preserve the complete behavioural repertoire, and is also inevitable, due to the ubiquity of activity-dependent CNS plasticity. Explorations of spinal cord plasticity are necessary for understanding motor skills. Furthermore, the spinal cord's comparative simplicity and accessibility makes it a logical starting point for studying skill acquisition. Induction and guidance of activity-dependent spinal cord plasticity will probably play an important role in realization of effective new rehabilitation methods for spinal cord injuries, cerebral palsy and other motor disorders.10aconditioning10aH-Reflex10aLearning10aMemory10amotor function10aplasticity10aRehabilitation10aspinal cord injury1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1725056601977nas a2200229   4500008004100000022001400041245005500055210004900110260001200159300001400171490000800185520137700193653001301570653001701583653001301600653001101613653001501624653001601639653002301655100002101678856004801699       2006                        eng d  a0079-612300aThe education and re-education of the spinal cord.0 aeducation and reeducation of the spinal cord  c02/2006  a261–2800 v1573 aIn normal life, activity-dependent plasticity occurs in the spinal cord as well as in the brain. Like CNS plasticity elsewhere, this spinal cord plasticity can occur at many neuronal and synaptic sites and by a variety of mechanisms. Spinal cord plasticity is prominent in postnatal development and contributes to acquisition of standard behaviors such as locomotion and rapid withdrawal from pain. Later on in life, spinal cord plasticity contributes to acquisition and maintenance of specialized motor skills, and to compensation for the peripheral and central changes associated with aging, disease, and trauma. Mastery of even the simplest behaviors is accompanied by complex spinal and supraspinal plasticity. This complexity is necessary, to preserve the full roster of behaviors, and is also inevitable, due to the ubiquity of activity-dependent plasticity in the CNS. Careful investigation of spinal cord plasticity is essential for understanding motor skills; and, because of the relative simplicity and accessibility of the spinal cord, is a logical and convenient starting point for exploring skill acquisition. Appropriate induction and guidance of activity-dependent plasticity in the spinal cord is likely to be a key part of the realization of effective new rehabilitation methods for spinal cord injuries, cerebral palsy, and other chronic motor disorders.10abehavior10aconditioning10aLearning10aMemory10aplasticity10aSpinal Cord10aspinal cord injury1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1716791601903nas a2200301   4500008004100000022001400041245010700055210006900162260001200231300001800243490000700261520101900268653002601287653001301313653001501326653001101341653001801352653001901370653002301389653002701412100001301439700002101452700002101473700001301494700002501507700002101532856004801553       2006                        eng d  a1529-240100aOperant conditioning of H-reflex can correct a locomotor abnormality after spinal cord injury in rats.0 aOperant conditioning of Hreflex can correct a locomotor abnormal  c11/2006  a12537–125430 v263 a<p>This study asked whether operant conditioning of the H-reflex can modify locomotion in spinal cord-injured rats. Midthoracic transection of the right lateral column of the spinal cord produced a persistent asymmetry in the muscle activity underlying treadmill locomotion. The rats were then either exposed or not exposed to an H-reflex up-conditioning protocol that greatly increased right soleus motoneuron response to primary afferent input, and locomotion was reevaluated. H-reflex up-conditioning increased the right soleus burst and corrected the locomotor asymmetry. In contrast, the locomotor asymmetry persisted in the control rats. These results suggest that appropriately selected reflex conditioning protocols might improve function in people with partial spinal cord injuries. Such protocols might be especially useful when significant regeneration becomes possible and precise methods for reeducating the regenerated spinal cord neurons and synapses are needed for restoring effective function.</p>10aH-reflex conditioning10aLearning10aLocomotion10aMemory10aMotor control10aRehabilitation10aspinal cord injury10aspinal cord plasticity1 aChen, Yi1 aChen, Xiang Yang1 aJakeman, Lyn, B.1 aChen, Lu1 aStokes, Bradford, T.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1713541502728nas a2200253   4500008004100000022001400041245003700055210003600092260001200128300001400140490000700154520210100161653002302262653001602285653001302301653001102314653001502325653001102340653001502351653001602366100002102382700002302403856004802426       2006                        eng d  a0301-008200aPlasticity from muscle to brain.0 aPlasticity from muscle to brain  c02/2006  a233–2630 v783 aRecognition that the entire central nervous system (CNS) is highly plastic, and that it changes continually throughout life, is a relatively new development. Until very recently, neuroscience has been dominated by the belief that the nervous system is hardwired and changes at only a few selected sites and by only a few mechanisms. Thus, it is particularly remarkable that Sir John Eccles, almost from the start of his long career nearly 80 years ago, focused repeatedly and productively on plasticity of many different kinds and in many different locations. He began with muscles, exploring their developmental plasticity and the functional effects of the level of motor unit activity and of cross-reinnervation. He moved into the spinal cord to study the effects of axotomy on motoneuron properties and the immediate and persistent functional effects of repetitive afferent stimulation. In work that combined these two areas, Eccles explored the influences of motoneurons and their muscle fibers on one another. He studied extensively simple spinal reflexes, especially stretch reflexes, exploring plasticity in these reflex pathways during development and in response to experimental manipulations of activity and innervation. In subsequent decades, Eccles focused on plasticity at central synapses in hippocampus, cerebellum, and neocortex. His endeavors extended from the plasticity associated with CNS lesions to the mechanisms responsible for the most complex and as yet mysterious products of neuronal plasticity, the substrates underlying learning and memory. At multiple levels, Eccles' work anticipated and helped shape present-day hypotheses and experiments. He provided novel observations that introduced new problems, and he produced insights that continue to be the foundation of ongoing basic and clinical research. This article reviews Eccles' experimental and theoretical contributions and their relationships to current endeavors and concepts. It emphasizes aspects of his contributions that are less well known at present and yet are directly relevant to contemporary issues.10aactivity-dependent10aJohn Eccles10aLearning10aMemory10amotor unit10amuscle10aplasticity10aSpinal Cord1 aWolpaw, Jonathan1 aCarp, Jonathan, S.  uhttp://www.ncbi.nlm.nih.gov/pubmed/1664718103537nas a2200253   4500008004100000022001400041245009500055210006900150260001200219300001200231490000800243520277200251653002903023653000803052653002703060653001303087653001403100653002403114100002603138700002603164700002403190700002103214856004803235       2005                        eng d  a1388-245700aBrain-computer interface (BCI) operation: signal and noise during early training sessions.0 aBraincomputer interface BCI operation signal and noise during ea  c01/2005  a56–620 v1163 aOBJECTIVE:
People can learn to control mu (8-12 Hz) or beta (18-25 Hz) rhythm amplitude in the electroencephalogram (EEG) recorded over sensorimotor cortex and use it to move a cursor to a target on a video screen. The recorded signal may also contain electromyogram (EMG) and other non-EEG artifacts. This study examines the presence and characteristics of EMG contamination during new users' initial brain-computer interface (BCI) training sessions, as they first attempt to acquire control over mu or beta rhythm amplitude and to use that control to move a cursor to a target.
METHODS:
In the standard one-dimensional format, a target appears along the right edge of the screen and 1s later the cursor appears in the middle of the left edge and moves across the screen at a fixed rate with its vertical movement controlled by a linear function of mu or beta rhythm amplitude. In the basic two-choice version, the target occupies the upper or lower half of the right edge. The user's task is to move the cursor vertically so that it hits the target when it reaches the right edge. The present data comprise the first 10 sessions of BCI training from each of 7 users. Their data were selected to illustrate the variations seen in EMG contamination across users.
RESULTS:
Five of the 7 users learned to change rhythm amplitude appropriately, so that the cursor hit the target. Three of these 5 showed no evidence of EMG contamination. In the other two of these 5, EMG was prominent in early sessions, and tended to be associated with errors rather than with hits. As EEG control improved over the 10 sessions, this EMG contamination disappeared. In the remaining two users, who never acquired actual EEG control, EMG was prominent in initial sessions and tended to move the cursor to the target. This EMG contamination was still detectable by Session 10.
CONCLUSIONS:
EMG contamination arising from cranial muscles is often present early in BCI training and gradually wanes. In those users who eventually acquire EEG control, early target-related EMG contamination may be most prominent for unsuccessful trials, and may reflect user frustration. In those users who never acquire EEG control, EMG may initially serve to move the cursor toward the target. Careful and comprehensive topographical and spectral analyses throughout user training are essential for detecting EMG contamination and differentiating between cursor control provided by EEG control and cursor control provided by EMG contamination.
SIGNIFICANCE:
Artifacts such as EMG are common in EEG recordings. Comprehensive spectral and topographical analyses are necessary to detect them and ensure that they do not masquerade as, or interfere with acquisition of, actual EEG-based cursor control.10abrain-computer interface10aEEG10aElectroencephalography10aLearning10amu rhythm10asensorimotor cortex1 aMcFarland, Dennis, J.1 aSarnacki, William, A.1 aVaughan, Theresa, M1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1558918402708nas a2200289   4500008004100000022001400041245010300055210006900158260001200227300001600239490000700255520184500262653002602107653001302133653001502146653002502161653001802186653001902204653002702223100001302250700002102263700002102284700001902305700002502324700002102349856004802370       2005                        eng d  a1529-240100aThe interaction of a new motor skill and an old one: H-reflex conditioning and locomotion in rats.0 ainteraction of a new motor skill and an old one Hreflex conditio  c07/2005  a6898–69060 v253 aNew and old motor skills can interfere with each other or interact in other ways. Because each skill entails a distributed pattern of activity-dependent plasticity, investigation of their interactions is facilitated by simple models. In a well characterized model of simple learning, rats and monkeys gradually change the size of the H-reflex, the electrical analog of the spinal stretch reflex. This study evaluates in normal rats the interactions of this new skill of H-reflex conditioning with the old well established skill of overground locomotion. In rats in which the soleus H-reflex elicited in the conditioning protocol (i.e., the conditioning H-reflex) had been decreased by down-conditioning, the H-reflexes elicited during the stance and swing phases of locomotion (i.e., the locomotor H-reflexes) were also smaller. Similarly, in rats in which the conditioning H-reflex had been increased by up-conditioning, the locomotor H-reflexes were also larger. Soleus H-reflex conditioning did not affect the duration, length, or right/left symmetry of the step cycle. However, the conditioned change in the stance H-reflex was positively correlated with change in the amplitude of the soleus locomotor burst, and the correlation was consistent with current estimates of the contribution of primary afferent input to the burst. Although H-reflex conditioning and locomotion did not interfere with each other, H-reflex conditioning did affect how locomotion was produced: it changed soleus burst amplitude and may have induced compensatory changes in the activity of other muscles. These results illustrate and clarify the subtlety and complexity of skill interactions. They also suggest that H-reflex conditioning might be used to improve the abnormal locomotion produced by spinal cord injury or other disorders of supraspinal control.10aH-reflex conditioning10aLearning10aLocomotion10amemory consolidation10aMotor control10aRehabilitation10aspinal cord plasticity1 aChen, Yi1 aChen, Xiang Yang1 aJakeman, Lyn, B.1 aSchalk, Gerwin1 aStokes, Bradford, T.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1603389902522nas a2200277   4500008004100000022001400041245008500055210006900140260001200209300001400221490000700235520169700242653003101939653002701970653001601997653001302013653001402026653002502040653001502065653001902080653002402099100002602123700002602149700002102175856004802196       2003                        eng d  a0301-051100aBrain-computer interface (BCI) operation: optimizing information transfer rates.0 aBraincomputer interface BCI operation optimizing information tra  c07/2003  a237–2510 v633 aPeople can learn to control mu (8-12 Hz) or beta (18-25 Hz) rhythm amplitude in the EEG recorded over sensorimotor cortex and use it to move a cursor to a target on a video screen. In the present version of the cursor movement task, vertical cursor movement is a linear function of mu or beta rhythm amplitude. At the same time the cursor moves horizontally from left to right at a fixed rate. A target occupies 50% (2-target task) to 20% (5-target task) of the right edge of the screen. The user's task is to move the cursor vertically so that it hits the target when it reaches the right edge. The goal of the present study was to optimize system performance. To accomplish this, we evaluated the impact on system performance of number of targets (i.e. 2-5) and trial duration (i.e. horizontal movement time from 1 to 4 s). Performance was measured as accuracy (percent of targets selected correctly) and also as bit rate (bits/min) (which incorporates, in addition to accuracy, speed and the number of possible targets). Accuracy declined as target number increased. At the same time, for six of eight users, four targets yielded the maximum bit rate. Accuracy increased as movement time increased. At the same time, the movement time with the highest bit rate varied across users from 2 to 4 s. These results indicate that task parameters such as target number and trial duration can markedly affect system performance. They also indicate that optimal parameter values vary across users. Selection of parameters suited both to the specific user and the requirements of the specific application is likely to be a key factor in maximizing the success of EEG-based communication and control.10aaugmentative communication10aElectroencephalography10ainformation10aLearning10amu rhythm10aoperant conditioning10aprosthesis10aRehabilitation10asensorimotor cortex1 aMcFarland, Dennis, J.1 aSarnacki, William, A.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1285316902878nas a2200241   4500008004100000022001400041245009400055210006900149260001200218300001200230490000800242520217200250653001802422653001902440653001302459653001502472653002302487100002102510700002302531700001302554700002102567856004802588       2002                        eng d  a0014-481900aCorticospinal tract transection prevents operantly conditioned H-reflex increase in rats.0 aCorticospinal tract transection prevents operantly conditioned H  c05/2002  a88–940 v1443 aOperant 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 > 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.10adorsal column10alateral column10aLearning10aplasticity10aspinal cord injury1 aChen, Xiang Yang1 aCarp, Jonathan, S.1 aChen, Lu1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1197676203278nas a2200229   4500008004100000022001400041245006900055210006700124260001200191300001400203490000700217520263700224653001302861653001702874653001302891653001102904653001902915653002302934100002102957700002202978856004803000       2001                        eng d  a0147-006X00aActivity-dependent spinal cord plasticity in health and disease.0 aActivitydependent spinal cord plasticity in health and disease  c03/2001  a807–8430 v243 aActivity-dependent plasticity occurs in the spinal cord throughout life. Driven by input from the periphery and the brain, this plasticity plays an important role in the acquisition and maintenance of motor skills and in the effects of spinal cord injury and other central nervous system disorders. The responses of the isolated spinal cord to sensory input display sensitization, long-term potentiation, and related phenomena that contribute to chronic pain syndromes; they can also be modified by both classical and operant conditioning protocols. In animals with transected spinal cords and in humans with spinal cord injuries, treadmill training gradually modifies the spinal cord so as to improve performance. These adaptations by the isolated spinal cord are specific to the training regimen and underlie new approaches to restoring function after spinal cord injury. Descending inputs from the brain that occur during normal development, as a result of supraspinal trauma, and during skill acquisition change the spinal cord. The early development of adult spinal cord reflex patterns is driven by descending activity; disorders that disrupt descending activity later in life gradually change spinal cord reflexes. Athletic training, such as that undertaken by ballet dancers, is associated with gradual alterations in spinal reflexes that appear to contribute to skill acquisition. Operant conditioning protocols in animals and humans can produce comparable reflex changes and are associated with functional and structural plasticity in the spinal cord, including changes in motoneuron firing threshold and axonal conduction velocity, and in synaptic terminals on motoneurons. The corticospinal tract has a key role in producing this plasticity. Behavioral changes produced by practice or injury reflect the combination of plasticity at multiple spinal cord and supraspinal sites. Plasticity at multiple sites is both necessary-to insure continued performance of previously acquired behaviors-and inevitable-due to the ubiquity of the capacity for activity-dependent plasticity in the central nervous system. Appropriate induction and guidance of activity-dependent plasticity in the spinal cord is an essential component of new therapeutic approaches aimed at maximizing function after spinal cord injury or restoring function to a newly regenerated spinal cord. Because plasticity in the spinal cord contributes to skill acquisition and because the spinal cord is relatively simple and accessible, this plasticity is a logical and practical starting point for studying the acquisition and maintenance of skilled behaviors.10abehavior10aconditioning10aLearning10aMemory10aRehabilitation10aspinal cord injury1 aWolpaw, Jonathan1 aTennissen, A., M.  uhttp://www.ncbi.nlm.nih.gov/pubmed/1152091901999nas a2200253   4500008004100000022001400041245005300055210005100108260001200159300001200171490000800183520136000191653001701551653001301568653001101581653001501592653000801607653001101615653001601626100002101642700001301663700002101676856004801697       2001                        eng d  a0304-394000aTime course of H-reflex conditioning in the rat.0 aTime course of Hreflex conditioning in the rat  c04/2001  a85–880 v3023 aThis 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.10aconditioning10aLearning10aMemory10aplasticity10arat10aReflex10aSpinal Cord1 aChen, Xiang Yang1 aChen, Lu1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1129039301573nas a2200229   4500008004100000022001400041245004600055210004100101260001200142300001400154490000700168520098800175653001301163653001301176653001101189653002501200653001501225653001601240653001901256100002101275856004701296       1997                        eng d  a0166-223600aThe complex structure of a simple memory.0 acomplex structure of a simple memory  c12/1997  a588–5940 v203 aOperant conditioning of the vertebrate H-reflex, which appears to be closely related to learning that occurs in real life, is accompanied by plasticity at multiple sites. Change occurs in the firing threshold and conduction velocity of the motoneuron, in several different synaptic terminal populations on the motoneuron, and probably in interneurons as well. Change also occurs contralaterally. The corticospinal tract probably has an essential role in producing this plasticity. While certain of these changes, such as that in the firing threshold, are likely to contribute to the rewarded behavior (primary plasticity), others might preserve previously learned behaviors (compensatory plasticity), or are simply activity-driven products of change elsewhere (reactive plasticity). As these data and those from other simple vertebrate and invertebrate models indicate, a complex pattern of plasticity appears to be the necessary and inevitable outcome of even the simplest learning.10aH-Reflex10aLearning10aMemory10aoperant conditioning10aplasticity10aSpinal Cord10astretch reflex1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/941667301682nas a2200229   4500008004100000022001400041245010100055210006900156260001200225300001400237490000800251520101200259653002101271653001301292653001301305653001101318653002501329653000901354100002101363700002101384856004701405       1995                        eng d  a0304-394000aOperantly conditioned plasticity and circadian rhythm in rat H-reflex are independent phenomena.0 aOperantly conditioned plasticity and circadian rhythm in rat Hre  c08/1995  a109–1120 v1953 aRecent studies indicate that rats can increase or decrease H-reflex amplitude in response to an operant conditioning paradigm. In addition, rats also display a circadian rhythm in H-reflex amplitude. As part of the development of H-reflex conditioning in the rat as a new model for defining the plasticity underlying a simple form of learning, this study examined the relationship in the rat between operantly conditioned H-reflex change and the H-reflex circadian rhythm. When H-reflex amplitude increased or decreased in response to the operant conditioning program, its circadian rhythm showed no changes in phase and minimal change in amplitude. Furthermore, animals did not alter daily performance schedule so as to use the rhythm to increase reward probability. Thus, in the rat, H-reflex operant conditioning and the H-reflex circadian rhythm appear to be independent phenomena. The circadian rhythm should not be a significant complicating factor in studies of operantly conditioned H-reflex change.10acircadian rhythm10aH-Reflex10aLearning10aMemory10aoperant conditioning10aRats1 aChen, Xiang Yang1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/747826202070nas a2200241   4500008004100000022001400041245009400055210006900149260001200218300001600230490000700246520139200253653001701645653001301662653001101675653001801686653001501704653001201719653001601731653001301747100002101760856004701781       1994                        eng d  a0195-913100aAcquisition and maintenance of the simplest motor skill: investigation of CNS mechanisms.0 aAcquisition and maintenance of the simplest motor skill investig  c12/1994  a1475–14790 v263 aThe spinal stretch reflex (SSR), or tendon jerk, is the simplest behavior of the vertebrate nervous system. It is mediated primarily by a wholly spinal, two-neuron pathway. Recent studies from several laboratories have shown that primates, human and nonhuman, can gradually increase or decrease the size of the SSR when reward depends on such change. Evidence of this training remains in the spinal cord after all supraspinal influence is removed. Thus, the learning of this simple motor skill changes the spinal cord itself. Comparable spinal plasticity probably plays a role in the acquisition of many complex motor skills. Intracellular physiological and anatomical studies are seeking the location and nature of this spinal cord plasticity. Attention focuses on the most probable sites of change, the group Ia afferent synapse on the alpha motoneuron and the motoneuron itself. Results to date indicate that modifications are present at several places in the spinal cord. Current clinical studies are investigating the use of spinal cord adaptive plasticity as a basis for a new therapeutic approach to spasticity and other forms of abnormal spinal reflex function that result from spinal cord injury, stroke, or other neurological disorders. In the future, understanding of spinal reflex plasticity may lead to development of improved training methods for a variety of motor skills.10aconditioning10aLearning10aMemory10aMotor control10aplasticity10aprimate10aSpinal Cord10atraining1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/786988201213nas a2200313   4500008004100000022001400041245005000055210004500105300001400150490000700164520043400171653001300605653001000618653001700628653002100645653001300666653001100679653001500690653001100705653001200716653001100728653001600739653001600755653002200771653001500793100002100808700002300829856004700852       1993                        eng d  a0065-140000aThe volitional nature of the simplest reflex.0 avolitional nature of the simplest reflex  a103–1110 v533 aRecent studies suggest that none of the behaviors of the vertebrate CNS are fixed responses incapable of change. Even the simplest reflex of all, the two-neuron, monosynaptic spinal stretch reflex (SSR), undergoes adaptive change under appropriate circumstances. Operantly conditioned SSR change occurs gradually over days and weeks and is associated with a complex pattern of CNS plasticity at both spinal and supraspinal sites.10abehavior10aBrain10aconditioning10ahuman physiology10aLearning10aMemory10amotoneuron10anature10aprimate10aReflex10aSpinal Cord10aspinal site10asupra spinal site10avertebrate1 aWolpaw, Jonathan1 aCarp, Jonathan, S.  uhttp://www.ncbi.nlm.nih.gov/pubmed/831723801769nas a2200253   4500008004100000022001400041245010600055210006900161260001200230300001400242490000800256520104100264653001701305653001301322653001101335653001501346653001701361653001201378653001801390100002101408700002301429700001601452856004701468       1989                        eng d  a0304-394000aMemory traces in spinal cord produced by H-reflex conditioning: effects of post-tetanic potentiation.0 aMemory traces in spinal cord produced by Hreflex conditioning ef  c08/1989  a113–1190 v1033 aOperant conditioning of the wholly spinal, largely monosynaptic triceps surae H-reflex in monkeys causes changes in lumbosacral spinal cord that persist after removal of supraspinal influence. We evaluated the interaction between post-tetanic potentiation and these memory traces. Animals in which the triceps surae H-reflex in one leg had been increased or decreased by conditioning were deeply anesthetized, and monosynaptic reflexes to L6-S1 dorsal root stimulation were recorded before and after tetanization from both legs for 3 days after thoracic cord transection. Animals remained anesthetized throughout and were sacrificed by overdose. Reflex asymmetries consistent with the effect of H-reflex conditioning were present after transection and persisted through the 3 days of study. Tetanization affected conditioned leg and control leg reflexes similarly. This finding suggests that, while post-tetanic potentiation and probably H-reflex conditioning alter Ia synaptic transmission, the two phenomena have different mechanisms.10aconditioning10aLearning10aMemory10amotoneuron10apotentiation10aprimate10aspinal reflex1 aWolpaw, Jonathan1 aCarp, Jonathan, S.1 aLee, C., L.  uhttp://www.ncbi.nlm.nih.gov/pubmed/277985201794nas a2200253   4500008004100000022001400041245008600055210006900141260001200210300001200222490000700234520107100241653001301312653001101325653002401336653002501360653001501385653001601400653001801416100002101434700001601455700002201471856004701493       1989                        eng d  a0014-481900aOperant conditioning of primate triceps surae H-reflex produces reflex asymmetry.0 aOperant conditioning of primate triceps surae Hreflex produces r  c03/1989  a35–390 v753 aMonkeys are able to increase or decrease triceps surae H-reflex when reward depends on reflex amplitude. Operantly conditioned change occurs over weeks and produces persistent alterations in the lumbosacral spinal cord which should be technically accessible substrates of primate memory. Previous work monitored and conditioned triceps surae H-reflex in one leg. To determine whether H-reflex conditioning in one leg affects the control leg, the present study monitored H-reflexes in both legs while the reflex in one leg underwent HR increases or HR decreases conditioning. Under the HR increases mode, H-reflex increase was much greater in the HR increases leg than in the control leg. Under the HR decreases mode, H-reflex decrease was confined to the HR decreases leg. By showing that conditioning of one leg's H-reflex produces H-reflex asymmetry, the data further define the phenomenon and indicate that the other leg can serve as an internal control for physiologic and anatomic studies exploring the sites and mechanisms of the spinal cord memory substrates.10aLearning10aMemory10amonosynaptic reflex10aoperant conditioning10aplasticity10aSpinal Cord10aspinal reflex1 aWolpaw, Jonathan1 aLee, C., L.1 aCalaitges, J., G.  uhttp://www.ncbi.nlm.nih.gov/pubmed/270735401400nas a2200253   4500008004100000022001400041245007800055210006900133260001200202300001400214490000700228520067600235653002200911653001300933653001300946653001100959653002500970653001500995653003501010653001801045100002101063700001501084856004701099       1988                        eng d  a0013-469400aOperant conditioning of primate spinal reflexes: effect on cortical SEPs.0 aOperant conditioning of primate spinal reflexes effect on cortic  c04/1988  a398–4010 v693 aPrevious studies have demonstrated operant conditioning of the primate spinal stretch reflex (SSR) and of its electrical analog, the H-reflex. We studied the evoked potential recorded over primary somatosensory cortex (SEP) which accompanies the H-reflex to determine whether the initial cortical response changes in the course of conditioned H-reflex change. When H-reflex amplitude changed, SEP amplitude also changed, but only half as much as the H-reflex. The results indicate that, while operant conditioning of the H-reflex has its largest effect on the spinal pathway of the reflex, it also has some effect on supraspinal pathways of the initial cortical response.10acortical response10aH-Reflex10aLearning10aMemory10aoperant conditioning10aplasticity10asomatosensory evoked potential10aspinal reflex1 aWolpaw, Jonathan1 aDowman, R.  uhttp://www.ncbi.nlm.nih.gov/pubmed/245073901726nas a2200217   4500008004100000022001400041245009000055210006900145260001200214300001400226490000600240520110600246653001301352653001101365653001501376653001201391653001801403653001901421100002101440856004701461       1985                        eng d  a0272-434000aAdaptive plasticity in the spinal stretch reflex: an accessible substrate of memory?.0 aAdaptive plasticity in the spinal stretch reflex an accessible s  c06/1985  a147–1650 v53 aThe study of the substrates of memory in higher vertebrates is one of the major problems of neurobiology. A simple and technically accessible experimental model is needed. Recent studies have demonstrated long-term adaptive plasticity, a form of memory, in the spinal stretch reflex (SSR). The SSR is due largely to a two-neuron monosynaptic arc, the simplest, best-defined, and most accessible pathway in the primate central nervous system (CNS). Monkeys can slowly change SSR amplitude without a change in initial muscle length or alpha motoneuron tone, when reward is made contingent on amplitude. Change occurs over weeks and months and persists for long periods. It is relatively specific to the agonist muscle and affects movement. The salient features of SSR adaptive plasticity, combined with clinical and laboratory evidence indicating spinal cord capacity for intrinsic change, suggest that SSR change eventually involves persistent segmental alteration. If this is the case, SSR plasticity should be a powerful model for studying the neuronal and synaptic substrates of memory in a primate.10aLearning10aMemory10aplasticity10aprimate10aspinal reflex10astretch reflex1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/316161601147nas a2200253   4500008004100000022001400041245010300055210006900158260001200227300001400239490000700253520041700260653001300677653001100690653001500701653001200716653001800728653001900746100002100765700002000786700002000806700002000826856004700846       1985                        eng d  a0304-394000aReduced day-to-day variation accompanies adaptive plasticity in the primate spinal stretch reflex.0 aReduced daytoday variation accompanies adaptive plasticity in th  c03/1985  a165–1710 v543 aMonkeys can change the amplitude of the spinal stretch reflex (SSR), or M1, when reward is made contingent on amplitude. The present study demonstrates that reduced SSR day-to-day variation accompanies such adaptive SSR change. This finding supports the assumption that initial, phase I, SSR change results from contingency-appropriate stabilization of tonic activity in relevant descending spinal cord pathways.10aLearning10aMemory10aplasticity10aprimate10aspinal reflex10astretch reflex1 aWolpaw, Jonathan1 aO'Keefe, J., A.1 aKieffer, V., A.1 aSanders, M., G.  uhttp://www.ncbi.nlm.nih.gov/pubmed/399105702097nas a2200241   4500008004100000022001400041245010700055210006900162260001200231300001400243490000800257520138500265653002401650653001901674653001301693653001101706653001201717653001901729100002101748700001901769700002001788856004701808       1984                        eng d  a0006-899300aAdaptive plasticity and diurnal rhythm in the primate spinal stretch reflex are independent phenomena.0 aAdaptive plasticity and diurnal rhythm in the primate spinal str  c05/1984  a385–3910 v3003 aRecent studies have revealed two phenomena producing considerable variation in amplitude of the initial, purely segmental, largely monosynaptic, response to sudden muscle stretch, the spinal stretch reflex (SSR), without change in background EMG activity or initial muscle length. The first is small and short-term, a modest diurnal rhythm in SSR amplitude. The second is large and long-term, marked adaptive change in SSR amplitude which occurs gradually over weeks and months when animals are rewarded for such change. This second phenomenon may involve persistent segmental alteration, and, if so, could constitute a technically accessible substrate of memory. The present study compared the two phenomena and sought evidence of interaction between them. The diurnal rhythm persisted, without change in phase and with only minimal change in amplitude, despite the occurrence of marked adaptive change. Animals did not utilize the rhythm to increase reward percentage by altering daily performance schedules. These results suggest that the mechanisms of the diurnal rhythm and of adaptive plasticity in SSR amplitude are separate and independent. The diurnal rhythm's effect on movement was not altered by adaptive change in SSR amplitude. This effect was comparable to adaptive change's effect on movement when both were expressed as change in movement/change in SSR amplitude.10aadaptive plasticity10adiurnal rhythm10aLearning10aMemory10aprimate10astretch reflex1 aWolpaw, Jonathan1 aNoonan, P., A.1 aO'Keefe, J., A.  uhttp://www.ncbi.nlm.nih.gov/pubmed/653963401504nas a2200217   4500008004100000022001400041245009100055210006900146260001200215300001400227490000800241520088100249653001301130653001101143653001501154653001201169653001801181653001901199100002101218856004701239       1983                        eng d  a0006-899300aAdaptive plasticity in the primate spinal stretch reflex: reversal and re-development.0 aAdaptive plasticity in the primate spinal stretch reflex reversa  c11/1983  a299–3040 v2783 aMonkeys can gradually increase or decrease the amplitude of the segmentally mediated spinal stretch reflex (SSR) without change in initial muscle length or background EMG activity. Both increase (under the SSR increases mode) and decrease (under the SSR decreases mode) occur slowly, progressing steadily over weeks. The present study investigated reversal and re-development of SSR amplitude change. Over a period of months, following collection of control data, monkeys were exposed to one mode, then to the other, and then to the first mode again. Development, reversal, and re-development of change all took place over weeks, following very similar courses. These data are consistent with the hypothesis that persistent segmental alteration underlies SSR amplitude change. Such persistent segmental alteration would constitute a technically accessible substrate of memory.10aLearning10aMemory10aplasticity10aprimate10aspinal reflex10astretch reflex1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/664032001114nas a2200265   4500008004100000022001400041245005400055210005300109260001200162300001400174490000800188520041600196653001300612653001100625653001500636653001200651653001800663653001900681100002100700700002000721700001900741700002100760700002000781856004700801       1983                        eng d  a0006-899300aAdaptive plasticity in the spinal stretch reflex.0 aAdaptive plasticity in the spinal stretch reflex  c05/1983  a196–2000 v2673 aMonkeys can change the amplitude of the spinal stretch reflex without change in initial alpha motor neuron tone, as measured by EMG, or in initial muscle length. Change is apparent in 5-10 days, continues to develop over weeks, and persists during inactive periods. Spinal stretch reflex change may be a valuable system for studying the neuronal and synaptic bases of an adaptive change in primate CNS function.10aLearning10aMemory10aplasticity10aprimate10aspinal reflex10astretch reflex1 aWolpaw, Jonathan1 aKieffer, V., A.1 aSeegal, R., F.1 aBraitman, D., J.1 aSanders, M., G.  uhttp://www.ncbi.nlm.nih.gov/pubmed/6860948