02425nas 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/2514354202704nas 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/1865718402003nas 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/1716791602175nas 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/1642042401903nas 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/1713541502190nas a2200253   4500008004100000022001400041245009500055210006900150260001200219300001600231490000800247520145200255653001301707653001501720653001101735653001501746653001601761100002501777700001901802700002201821700002101843700002401864856004801888       2006                        eng d  a1388-245700aPlastic changes in the human H-reflex pathway at rest following skillful cycling training.0 aPlastic changes in the human Hreflex pathway at rest following s  c08/2006  a1682–16910 v1173 aOBJECTIVE:
The spinal cord is capable of activity-dependent plasticity, but the extent of its participation in human motor learning is not known. Here, we tested the hypothesis that acquisition of a locomotor-related skill modulates the pathway of the H-reflex, a measure of spinal cord excitability that is susceptible to plastic changes.
METHODS:
Subjects were tested on their ability to establish a constant cycling speed on a recumbent bike despite frequent changes in pedal resistance. The coefficient of variation of speed (CV(speed)) measured their ability to acquire this skill (decreasing CV(speed) with training reflects performance improvements). Soleus H-reflexes were taken at rest before and after cycling.
RESULTS:
Ability to establish a target speed increased and H-reflex size decreased more after cycling training involving frequent changes in pedal resistance that required calibrated locomotor compensatory action than with training involving constant pedal resistances and lesser compensation. The degree of performance improvement correlated with the reduction in the amplitude of the H-reflex.
CONCLUSIONS:
Skillful establishment of a constant cycling speed despite changing pedal resistances is associated with persistent modulation of activity in spinal pathways.
SIGNIFICANCE:
Recalibration of activity in the H-reflex pathway may be part of the control strategy required for locomotor-related skill acquisition.10aH-Reflex10aLocomotion10aMemory10aplasticity10aSpinal Cord1 aMazzocchio, Riccardo1 aKitago, Tomoko1 aLiuzzi, Gianpiero1 aWolpaw, Jonathan1 aCohen, Leonardo, G.  uhttp://www.ncbi.nlm.nih.gov/pubmed/1679333302728nas 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/1664718103278nas 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/1152091902143nas a2200217   4500008004100000022001400041245008000055210006900135260001200204300001400216490000800230520152500238653001701763653001301780653001101793653001501804653001601819100002101835700002101856856004801877       2001                        eng d  a0014-481900aOperant conditioning of rat H-reflex: effects on mean latency and duration.0 aOperant conditioning of rat Hreflex effects on mean latency and   c01/2001  a274–2790 v1363 aWe are currently studying the mechanisms of operantly conditioned changes in the H-reflex in the rat. Primate data suggest that H-reflex decrease is due to a positive shift in motoneuron firing threshold and a small decrease in the monosynaptic excitatory postsynaptic potential (EPSP), and that increase might be due to change in group-I oligosynaptic (especially disynaptic) input. To further evaluate the possibility of conditioned change in oligosynaptic input, we compared the mean latency (i.e., the average latency of the entire H-reflex) and the duration of control (i.e., pre-conditioning) H-reflexes with those of H-reflexes after up-conditioning or down-conditioning. Up-conditioning was associated with small, statistically significant increases in H-reflex mean latency [+0.11+/-0.05 (+/-SE) ms] and duration (+0.32+/-0.16 ms). The mean latency of the H-reflex increase (i.e., the part added to the H-reflex by up-conditioning) was 0.28+/-0.14 (+/-SE) ms greater than that of the control H-reflex. Down-conditioning had no significant effect on mean latency or duration. While these results indicate that operant conditioning does not greatly change H-reflex mean latency or duration, the effects detected with up-conditioning are consistent with the hypothesis that decreased inhibition, or increased excitation, by homonymous and heteronymous group-I oligosynaptic input contributes to the H-reflex increase produced by up-conditioning. Several other mechanisms might also account for these small effects.10aconditioning10aH-Reflex10aMemory10aplasticity10aSpinal Cord1 aWolpaw, Jonathan1 aChen, Xiang Yang  uhttp://www.ncbi.nlm.nih.gov/pubmed/1120629101999nas 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/831723801398nas a2200241   4500008004100000022001400041245006300055210006100118260001200179300001400191490000700205520074600212653001700958653001300975653001100988653001500999653001201014653001801026653001901044100002101063700002501084856004701109       1990                        eng d  a0165-027000aOperant conditioning of H-reflex in freely moving monkeys.0 aOperant conditioning of Hreflex in freely moving monkeys  c02/1990  a145–1520 v313 aThe H-reflex, the electrical analog of the stretch reflex or tendon jerk, is the simplest behavior of the primate CNS. It is subserved by a wholly spinal two-neuron reflex arc. Recent studies show that this reflex can be increased or decreased by operant conditioning, and that such conditioning causes plastic changes in the spinal cord itself. Thus, H-reflex conditioning provides a powerful new model for investigating primate memory traces. The key feature of this model, the conditioning task, originally required animal restraint. This report describes a new tether-based design that allows H-reflex measurement and conditioning without restraint. This design integrates the conditioning task into the life of the freely moving animal.10aconditioning10aH-Reflex10aMemory10aplasticity10aprimate10aspinal reflex10astretch reflex1 aWolpaw, Jonathan1 aHerchenroder, P., A.  uhttp://www.ncbi.nlm.nih.gov/pubmed/231981501769nas 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