02092nas 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/2463695402012nas a2200229   4500008004100000022001400041245004900055210004800104260001200152300001100164490000800175520137600183653003401559653001301593653002501606653001901631653002301650653001801673100002201691700002101713856004801734       2015                        eng d  a1875-785500aTargeted neuroplasticity for rehabilitation.0 aTargeted neuroplasticity for rehabilitation  c03/2015  a157-720 v2183 a<p>An operant-conditioning protocol that bases reward on the electromyographic response produced by a specific CNS pathway can change that pathway. For example, in both animals and people, an operant-conditioning protocol can increase or decrease the spinal stretch reflex or its electrical analog, the H-reflex. Reflex change is associated with plasticity in the pathway of the reflex as well as elsewhere in the spinal cord and brain. Because these pathways serve many different behaviors, the plasticity produced by this conditioning can change other behaviors. Thus, in animals or people with partial spinal cord injuries, appropriate reflex conditioning can improve locomotion. Furthermore, in people with spinal cord injuries, appropriate reflex conditioning can trigger widespread beneficial plasticity. This wider plasticity appears to reflect an iterative process through which the multiple behaviors in the individual's repertoire negotiate the properties of the spinal neurons and synapses that they all use. Operant-conditioning protocols are a promising new therapeutic method that could complement other rehabilitation methods and enhance functional recovery. Their successful use requires strict adherence to appropriately designed procedures, as well as close attention to accommodating and engaging the individual subject in the conditioning process.</p>10aactivity-dependent plasticity10aH-Reflex10aoperant conditioning10aRehabilitation10aspinal cord injury10aspinal reflex1 aThompson, Aiko, K1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/2589013602145nas a2200217   4500008004100000022001400041245008500055210006900140260001200209300000700221490000600228520150000234653001301734653002401747653001501771653002301786653002701809100002201836700002101858856004801879       2014                        eng d  a1662-514500aOperant conditioning of spinal reflexes: from basic science to clinical therapy.0 aOperant conditioning of spinal reflexes from basic science to cl  c03/2014  a250 v83 aNew appreciation of the adaptive capabilities of the nervous system, recent recognition that most spinal cord injuries are incomplete, and progress in enabling regeneration are generating growing interest in novel rehabilitation therapies. Here we review the 35-year evolution of one promising new approach, operant conditioning of spinal reflexes. This work began in the late 1970's as basic science; its purpose was to develop and exploit a uniquely accessible model for studying the acquisition and maintenance of a simple behavior in the mammalian central nervous system (CNS). The model was developed first in monkeys and then in rats, mice, and humans. Studies with it showed that the ostensibly simple behavior (i.e., a larger or smaller reflex) rests on a complex hierarchy of brain and spinal cord plasticity; and current investigations are delineating this plasticity and its interactions with the plasticity that supports other behaviors. In the last decade, the possible therapeutic uses of reflex conditioning have come under study, first in rats and then in humans. The initial results are very exciting, and they are spurring further studies. At the same time, the original basic science purpose and the new clinical purpose are enabling and illuminating each other in unexpected ways. The long course and current state of this work illustrate the practical importance of basic research and the valuable synergy that can develop between basic science questions and clinical needs.10aH-Reflex10alearning and memory10aLocomotion10aspinal cord injury10aspinal cord plasticity1 aThompson, Aiko, K1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/2467244102425nas 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/2514354201519nas a2200301   4500008004100000022001400041245009500055210006900150260001200219300001400231490001700245520064100262653001300903653002400916653001500940653001500955653002400970653001900994653002301013100002101036700001301057700001301070700001901083700002301102700002301125700002101148856004801169       2010                        eng d  a1749-663200aReflex conditioning: a new strategy for improving motor function after spinal cord injury.0 aReflex conditioning a new strategy for improving motor function   c06/2010  aE12–E210 v1198 Suppl 13 aSpinal reflex conditioning changes reflex size, induces spinal cord plasticity, and modifies locomotion. Appropriate reflex conditioning can improve walking in rats after spinal cord injury (SCI). Reflex conditioning offers a new therapeutic strategy for restoring function in people with SCI. This approach can address the specific deficits of individuals with SCI by targeting specific reflex pathways for increased or decreased responsiveness. In addition, once clinically significant regeneration can be achieved, reflex conditioning could provide a means of reeducating the newly (and probably imperfectly) reconnected spinal cord.10aH-Reflex10alearning and memory10aLocomotion10aplasticity10areflex conditioning10aRehabilitation10aspinal cord injury1 aChen, Xiang Yang1 aChen, Yi1 aWang, Yu1 aThompson, Aiko1 aCarp, Jonathan, S.1 aSegal, Richard, L.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/2059053402003nas 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/1725056602272nas a2200253   4500008004100000022001400041245009400055210006900149260001200218300001600230490000700246520153000253653002401783653002601807653001501833653000801848653002301856100002101879700001301900700001301913700002301926700002101949856004801970       2006                        eng d  a0897-715100aCorticospinal tract transection permanently abolishes H-reflex down-conditioning in rats.0 aCorticospinal tract transection permanently abolishes Hreflex do  c11/2006  a1705–17120 v233 aPrevious studies have shown that corticospinal tract (CST) transection, but not transection of other major spinal cord tracts, prevents down-conditioning of the H-reflex, the electrical analog of the spinal stretch reflex. This study set out to determine whether the loss of the capacity for H-reflex down-conditioning caused by CST transection is permanent. Female Sprague-Dawley rats received CST, lateral column (LC), or dorsal column ascending tract (DA) transection at T8-9; 9-10 months later, they were exposed to the H-reflex down-conditioning protocol for 50 days. In the LC and DA rats, H-reflex size fell to 60 (+/- 9 SEM)% and 60 (+/- 19)%, respectively, of its initial size. This down-conditioning was comparable to that of normal rats. In contrast, H-reflex size in the CST rats rose to 170 (+/- 42)% of its initial size. A similar rise does not occur in rats exposed to down-conditioning shortly after CST transection. These results indicate that CST transection permanently eliminates the capacity for H-reflex down-conditioning and has gradual long-term effects on sensorimotor cortex function. They imply that H-reflex down-conditioning can be a reliable measure of CST function for long-term studies of the effects of spinal cord injury and/or for evaluations of the efficacy of experimental therapeutic procedures, such as those intended to promote CST regeneration. The results also suggest that the role of sensorimotor cortex in down-conditioning extends beyond generation of the essential CST activity.10acorticospinal tract10aH-reflex conditioning10aplasticity10arat10aspinal cord injury1 aChen, Xiang Yang1 aChen, Yi1 aChen, Lu1 aTennissen, Ann, M.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1711591501977nas 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/1713541502878nas 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/1197676201877nas a2200253   4500008004100000022001400041245007900055210006900134260001200203300001400215490000800229520115300237653002201390653002401412653001901436653001301455653000801468653002301476100002101499700001301520700002101533700002101554856004801575       2002                        eng d  a0006-899300aCorticospinal tract transection reduces H-reflex circadian rhythm in rats.0 aCorticospinal tract transection reduces Hreflex circadian rhythm  c06/2002  a101–1080 v9423 aIn freely moving rats and monkeys, H-reflex amplitude displays a marked circadian variation without change in background motoneuron tone. In rats, the H-reflex is largest around noon and smallest around midnight. The present study evaluated in rats the effects on this rhythm of calibrated contusions of mid-thoracic spinal cord and mid-thoracic transection of specific spinal cord pathways. In 33 control rats, rhythm amplitude averaged 29.0(+/-2.6 S.E.)% of H-reflex amplitude. Contusion injuries at T8-9 that destroyed 53-88% of the white matter significantly reduced the rhythm to 18.9(+/-2.4)% of H-reflex amplitude. Transection of the ipsilateral lateral column, which contains the rubrospinal, vestibulospinal, and reticulospinal tracts, or bilateral transection of the dorsal column ascending tract did not affect rhythm amplitude or phase. In contrast, bilateral transection of the main corticospinal tract significantly reduced the rhythm to 14.7(+/-6.6)%. These results indicate that the H-reflex circadian rhythm depends in part on descending influence from the brain and that this influence is conveyed by the main corticospinal tract.10acircadian rhythms10acorticospinal tract10adiurnal rhythm10aH-Reflex10arat10aspinal cord injury1 aChen, Xiang Yang1 aChen, Lu1 aWolpaw, Jonathan1 aJakeman, Lyn, B.  uhttp://www.ncbi.nlm.nih.gov/pubmed/1203185803278nas 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/1152091902808nas a2200277   4500008004100000022001400041245011500055210006900170260001200239300001400251490000700265520196900272653002402241653001802265653003402283653001902317653000802336653002002344653002302364100002102387700002202408700001302430700001802443700002102461856004802482       2001                        eng d  a0897-715100aShort-Term and medium-term effects of spinal cord tract transections on soleus H-reflex in freely moving rats.0 aShortTerm and mediumterm effects of spinal cord tract transectio  c03/2001  a313–3270 v183 aSpinal cord function is normally influenced by descending activity from supraspinal structures. When injury removes or distorts this influence, function changes and spasticity and other disabling problems eventually appear. Understanding how descending activity affects spinal cord function could lead to new means for inducing, guiding, and assessing recovery after injury. In this study, we investigated the short-term and medium-term effects of spinal cord bilateral dorsal column (DC), unilateral (ipsilateral) lateral column (LC), bilateral dorsal column ascending tract (DA), or bilateral dorsal column corticospinal tract (CST) transection at vertebral level T8-T9 on the soleus H-reflex in freely moving rats. Data were collected continuously for 10-20 days before and for 20-155 days after bilateral DC (13 rats), DA (10 rats), CST (eight rats), or ipsilateral LC (seven rats) transection. Histological examination showed that transections were 98(+/- 3 SD)% complete for DC rats, 80(+/- 20)% complete for LC rats, 91(+/- 13 SD)% complete for DA rats, and 95(+/-13)% complete for CST rats. LC, CST, and DA transections produced an immediate (i.e., first-day) increase in H-reflex amplitude. LC transection also produced a small decrease in background activity in the first few posttransection days. Other than this small decrease, none of the transections produced evidence for the phenomenon of spinal shock. For all transections, all measures returned to or neared pretransection values within 2 weeks. DA and LC transections were associated with modest increase in H-reflex amplitude 1-3 months after transection. These medium-term effects must be taken into account when assessing transection effects on operant conditioning of the H-reflex. At the same time, the results are consistent with other evidence that, while H-reflex rate dependence and H-reflex operant conditioning are sensitive measures of spinal cord injury, the H-reflex itself is not.10acorticospinal tract10adorsal column10adorsal column ascending tract10alateral column10arat10asoleus activity10aspinal cord injury1 aChen, Xiang Yang1 aFeng-Chen, K., C.1 aChen, Lu1 aStark, D., M.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1128455102520nas a2200253   4500008004100000022001400041245007700055210007100132260001200203300001400215490000700229520179900236653001302035653002502048653001502073653000802088653001802096653002302114100002102137700002102158700002002179700001902199856004802218       1999                        eng d  a0897-715100aOperant conditioning of H-reflex increase in spinal cord–injured rats.0 aOperant conditioning of Hreflex increase in spinal cord–injured   c02/1999  a175–1860 v163 aOperant conditioning of the spinal stretch reflex or its electrical analog, the H-reflex, is a new model for exploring the mechanisms of long-term supraspinal control over spinal cord function. Primates and rats can gradually increase (HRup conditioning mode) or decrease (HRdown conditioning mode) the H-reflex when reward is based on H-reflex amplitude. An earlier study indicated that HRdown conditioning of the soleus H-reflex in rats is impaired following contusion injury to thoracic spinal cord. The extent of impairment was correlated with the percent of white matter lost at the injury site. The present study investigated the effects of spinal cord injury on HRup conditioning. Soleus H-reflexes were elicited and recorded with chronically implanted electrodes from 14 rats that had been subjected to calibrated contusion injuries to the spinal cord at T8. At the lesion epicenter, 12-39% of the white matter remained. After control-mode data were collected, each rat was exposed to the HRup conditioning mode for 50 days. Final H-reflex amplitudes after HRup conditioning averaged 112% (+/-22% SD) of control. This value was significantly smaller than that for 13 normal rats exposed to HRup conditioning, in which final amplitude averaged 153% (+/-51%) SD of control. As previously reported for HRdown conditioning after spinal cord injury, success was inversely correlated with the severity of the injury as assessed by white matter preservation and by time to return of bladder function. HRup and HRdown conditioning are similarly sensitive to injury. These results further demonstrate that H-reflex conditioning is a sensitive measure of the long-term effects of injury on supraspinal control over spinal cord functions and could prove a valuable measure of therapeutic efficacy.10aH-Reflex10aoperant conditioning10aplasticity10arat10asoleus muscle10aspinal cord injury1 aChen, Xiang Yang1 aWolpaw, Jonathan1 aJakeman, L., B.1 aStokes, B., T.  uhttp://www.ncbi.nlm.nih.gov/pubmed/1009896202267nas a2200253   4500008004100000022001400041245006600055210006300121260001200184300001400196490000700210520156600217653001301783653002501796653001501821653000801836653001801844653002301862100002101885700002101906700002001927700001901947856004701966       1996                        eng d  a0897-715100aOperant conditioning of H-reflex in spinal cord-injured rats.0 aOperant conditioning of Hreflex in spinal cordinjured rats  c12/1996  a755–7660 v133 aOperant conditioning of the spinal stretch reflex or its electrical analog, the H-reflex, is a new model for exploring the mechanisms of supraspinal control over spinal cord function. Both rats and primates can gradually increase (HRup conditioning mode) or decrease (HRdown conditioning mode) soleus H-reflex magnitude when exposed to an operant conditioning task. This study used H-reflex operant conditioning to assess and modify spinal cord function after injury. Soleus H-reflexes were elicited and recorded with chronically implanted electrodes from rats that had been subjected to calibrated contusion injuries to the spinal cord at T8. From 18 to 140 days after injury, background EMG, M response amplitude, and initial H-reflex amplitude were not significantly different from those of normal rats. HRdown conditioning was successful in some, but not all, spinal cord-injured rats. The H-reflex decrease achieved by conditioning was inversely correlated with the severity of the injury as assessed histologically or by time to return of bladder function. It was not correlated with the length of time between injury and the beginning of conditioning. The results confirm the importance of descending control from supraspinal structures in mediating operantly conditioned change in H-reflex amplitude. In conjunction with recent human studies, they suggest that H-reflex conditioning could provide a sensitive new means for assessing spinal cord function after injury, and might also provide a method for initiating and guiding functional rehabilitation.10aH-Reflex10aoperant conditioning10aplasticity10arat10asoleus muscle10aspinal cord injury1 aChen, Xiang Yang1 aWolpaw, Jonathan1 aJakeman, L., B.1 aStokes, B., T.  uhttp://www.ncbi.nlm.nih.gov/pubmed/900206101361nas a2200229   4500008004100000022001400041245010600055210006900161260001200230300001400242490000700256520067400263653002400937653001200961653001600973653002300989653001801012653001701030100002101047700001601068856004701084       1987                        eng d  a0014-481900aMotoneuron response to dorsal root stimulation in anesthetized monkeys after spinal cord transection.0 aMotoneuron response to dorsal root stimulation in anesthetized m  c10/1987  a428–4330 v683 aIn preparation for studying the spinal cord alterations produced by operant conditioning of spinal reflexes, we studied peripheral nerve responses to supramaximal dorsal root stimulation in the lumbosacral cord of deeply anesthetized monkeys before and after thoracic cord transection. Except for variable depression in the first few minutes, reflex responses were not reduced or otherwise significantly affected by transection in the hour immediately following the lesion or for at least 50 h. The results suggest that reduction in muscle spindle sensitivity and/or in polysynaptic motoneuron excitation contributes to stretch reflex depression after cord transection.10amonosynaptic reflex10aprimate10aSpinal Cord10aspinal cord injury10aspinal reflex10aspinal shock1 aWolpaw, Jonathan1 aLee, C., L.  uhttp://www.ncbi.nlm.nih.gov/pubmed/3480233