02314nas a2200229   4500008004100000022001400041245010300055210006900158260001200227300001200239490000800251520162300259653002901882653001101911653001301922653001801935653001601953100002501969700002101994700002102015856004802036       2015                        eng d  a1522-159800aElectrocorticographic activity over sensorimotor cortex and motor function in awake behaving rats.0 aElectrocorticographic activity over sensorimotor cortex and moto  c04/2015  a2232-410 v1133 a<p>Sensorimotor cortex exerts both short-term and long-term control over the spinal reflex pathways that serve motor behaviors. Better understanding of this control could offer new possibilities for restoring function after central nervous system trauma or disease. We examined the impact of ongoing sensorimotor cortex (SMC) activity on the largely monosynaptic pathway of the H-reflex, the electrical analog of the spinal stretch reflex. In 41 awake adult rats, we measured soleus electromyographic (EMG) activity, the soleus H-reflex, and electrocorticographic activity over the contralateral SMC while rats were producing steady-state soleus EMG activity. Principal component analysis of electrocorticographic frequency spectra before H-reflex elicitation consistently revealed three frequency bands: μβ (5-30 Hz), low γ (γ1; 40-85 Hz), and high γ (γ2; 100-200 Hz). Ongoing (i.e., background) soleus EMG amplitude correlated negatively with μβ power and positively with γ1 power. In contrast, H-reflex size correlated positively with μβ power and negatively with γ1 power, but only when background soleus EMG amplitude was included in the linear model. These results support the hypothesis that increased SMC activation (indicated by decrease in μβ power and/or increase in γ1 power) simultaneously potentiates the H-reflex by exciting spinal motoneurons and suppresses it by decreasing the efficacy of the afferent input. They may help guide the development of new rehabilitation methods and of brain-computer interfaces that use SMC activity as a substitute for lost or impaired motor outputs.</p>10abrain-computer interface10acortex10aH-Reflex10aMotor control10aSpinal Cord1 aBoulay, Chadwick, B.1 aChen, Xiang Yang1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/2563207602675nas a2200325   4500008004100000022001400041245010000055210006900155260001200224300001200236490000800248520178700256653001202043653002602055653001102081653001302092653001302105653001502118653000902133653000902142653002502151653002502176100001302201700001302214700001902227700001302246700002102259700002102280856004802301       2014                        eng d  a1522-159800aLocomotor impact of beneficial or nonbeneficial H-reflex conditioning after spinal cord injury.0 aLocomotor impact of beneficial or nonbeneficial Hreflex conditio  c03/2014  a1249-580 v1113 aWhen new motor learning changes neurons and synapses in the spinal cord, it may affect previously learned behaviors that depend on the same spinal neurons and synapses. To explore these effects, we used operant conditioning to strengthen or weaken the right soleus H-reflex pathway in rats in which a right spinal cord contusion had impaired locomotion. When up-conditioning increased the H-reflex, locomotion improved. Steps became longer, and step-cycle asymmetry (i.e., limping) disappeared. In contrast, when down-conditioning decreased the H-reflex, locomotion did not worsen. Steps did not become shorter, and asymmetry did not increase. Electromyographic and kinematic analyses explained how H-reflex increase improved locomotion and why H-reflex decrease did not further impair it. Although the impact of up-conditioning or down-conditioning on the H-reflex pathway was still present during locomotion, only up-conditioning affected the soleus locomotor burst. Additionally, compensatory plasticity apparently prevented the weaker H-reflex pathway caused by down-conditioning from weakening the locomotor burst and further impairing locomotion. The results support the hypothesis that the state of the spinal cord is a "negotiated equilibrium" that serves all the behaviors that depend on it. When new learning changes the spinal cord, old behaviors undergo concurrent relearning that preserves or improves their key features. Thus, if an old behavior has been impaired by trauma or disease, spinal reflex conditioning, by changing a specific pathway and triggering a new negotiation, may enable recovery beyond that achieved simply by practicing the old behavior. Spinal reflex conditioning protocols might complement other neurorehabilitation methods and enhance recovery.10aAnimals10aConditioning, Operant10aFemale10aH-Reflex10aLearning10aLocomotion10aMale10aRats10aRats, Sprague-Dawley10aSpinal Cord Injuries1 aChen, Yi1 aChen, Lu1 aLiu, Rongliang1 aWang, Yu1 aChen, Xiang Yang1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/2437128801519nas a2200301   4500008004100000022001400041245009500055210006900150260001200219300001400231490001700245520064100262653001300903653002400916653001500940653001500955653002400970653001900994653002301013100002101036700001301057700001301070700001901083700002301102700002301125700002101148856004801169       2010                        eng d  a1749-663200aReflex conditioning: a new strategy for improving motor function after spinal cord injury.0 aReflex conditioning a new strategy for improving motor function   c06/2010  aE12–E210 v1198 Suppl 13 aSpinal reflex conditioning changes reflex size, induces spinal cord plasticity, and modifies locomotion. Appropriate reflex conditioning can improve walking in rats after spinal cord injury (SCI). Reflex conditioning offers a new therapeutic strategy for restoring function in people with SCI. This approach can address the specific deficits of individuals with SCI by targeting specific reflex pathways for increased or decreased responsiveness. In addition, once clinically significant regeneration can be achieved, reflex conditioning could provide a means of reeducating the newly (and probably imperfectly) reconnected spinal cord.10aH-Reflex10alearning and memory10aLocomotion10aplasticity10areflex conditioning10aRehabilitation10aspinal cord injury1 aChen, Xiang Yang1 aChen, Yi1 aWang, Yu1 aThompson, Aiko1 aCarp, Jonathan, S.1 aSegal, Richard, L.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/2059053402476nas a2200241   4500008004100000022001400041245011900055210006900174260001200243300001600255490000700271520173900278653001302017653001902030653001602049653002502065653001502090653001602105100002302121700002102144700002102165856004802186       2009                        eng d  a1529-240100aAcquisition of a simple motor skill: task-dependent adaptation plus long-term change in the human soleus H-reflex.0 aAcquisition of a simple motor skill taskdependent adaptation plu  c05/2009  a5784–57920 v293 aActivity-dependent plasticity occurs throughout the CNS. However, investigations of skill acquisition usually focus on cortex. To expand the focus, we analyzed in humans the development of operantly conditioned H-reflex change, a simple motor skill that develops gradually and involves plasticity in both the brain and the spinal cord. Each person completed 6 baseline and 24 conditioning sessions over 10 weeks. In each conditioning session, the soleus H-reflex was measured while the subject was or was not asked to increase (HRup subjects) or decrease (HRdown subjects) it. When the subject was asked to change H-reflex size, immediate visual feedback indicated whether a size criterion had been satisfied. Over the 24 conditioning sessions, H-reflex size gradually increased in six of eight HRup subjects and decreased in eight of nine HRdown subjects, resulting in final sizes of 140 +/- 12 and 69 +/- 6% of baseline size, respectively. The final H-reflex change was the sum of within-session (i.e., task-dependent) adaptation and across-session (i.e., long-term) change. Task-dependent adaptation appeared within four to six sessions and persisted thereafter, averaging +13% in HRup subjects and -15% in HRdown subjects. In contrast, long-term change began after 10 sessions and increased gradually thereafter, reaching +27% in HRup subjects and -16% in HRdown subjects. Thus, the acquisition of H-reflex conditioning consists of two phenomena, task-dependent adaptation and long-term change, that together constitute the new motor skill. In combination with previous data, this new finding further elucidates the interaction of plasticity in brain and spinal cord that underlies the acquisition and maintenance of motor skills.10aH-Reflex10amotor learning10amotor skill10aoperant conditioning10aplasticity10aSpinal Cord1 aThompson, Aiko, K.1 aChen, Xiang Yang1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1942024602175nas 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/1642042401877nas 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/1203185801678nas a2200277   4500008004100000022001400041245009700055210006900152260001200221300001000233490000800243520088300251653002201134653002101156653001301177653002501190653001601215653001501231653001801246653000801264100002301272700002101295700001501316700002101331856004801352       2001                        eng d  a0304-394000aEffects of chronic nerve cuff and intramuscular electrodes on rat triceps surae motor units.0 aEffects of chronic nerve cuff and intramuscular electrodes on ra  c10/2001  a1–40 v3123 aIn order to assess the long-term effects of implanted electrodes on motor unit properties, we studied triceps surae (TS) motor units in rats implanted for 3-10 months with a tibial nerve cuff electrode for H-reflex elicitation and intramuscular electrodes for recording TS electromyographic activity. Motor units with sag from implanted rats displayed greater tetanic force than those from unimplanted rats. Motor units without sag had shorter twitch contraction times. This disrupted the relationship between sag and contraction time that was always present in unimplanted rats. These differences were consistent with a small degree of muscle denervation and subsequent reinnervation. Further analyses ascribed this effect to the nerve cuff rather than to the intramuscular electrodes. Comparable changes in motor unit properties may occur in humans with implanted nerve cuffs.10achronic recording10acontraction time10aH-Reflex10aimplanted electrodes10amotor units10anerve cuff10areinnervation10asag1 aCarp, Jonathan, S.1 aChen, Xiang Yang1 aSheikh, H.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1157883102272nas a2200241   4500008004100000022001400041245007000055210006800125260001200193300001400205490000800219520158400227653001301811653002001824653002501844653001501869653001801884100002301902700002101925700001501946700002101961856004801982       2001                        eng d  a0014-481900aMotor unit properties after operant conditioning of rat H-reflex.0 aMotor unit properties after operant conditioning of rat Hreflex  c10/2001  a382–3860 v1403 aOperant conditioning of the H-reflex produces plasticity at several sites in the spinal cord, including the motoneuron. This study assessed whether this spinal cord plasticity is accompanied by changes in motor unit contractile properties. Thirty-one adult male Sprague-Dawley rats implanted for chronic recording of triceps surae electromyographic activity and H-reflex elicitation were exposed for at least 40 days to HRup or HRdown training, in which reward occurred when the H-reflex was greater than (12 HRup rats) or less than (12 HRdown rats) a criterion value, or continued under the control mode in which the H-reflex was simply measured (7 HRcon rats). At the end of H-reflex data collection, rats were anesthetized and the contractile properties of 797 single triceps surae motor units activated by intraaxonal (or intramyelin) current injection were determined. Motor units were classified as S, FR, Fint, or FF on the basis of sag and fatigue properties. Maximum tetanic force and twitch contraction time were also measured. HRdown rats exhibited a significant increase in the fatigue index of fast-twitch motor units. This resulted in a significant decrease in the percentage of Fint motor units and a significant increase in that of FR motor units. HRup conditioning had no effect on fatigue index. Neither HRup nor HRdown conditioning affected maximum tetanic force or twitch contraction time. These data are consistent with the hypothesis that conditioning mode-specific change in motoneuron firing patterns causes activity-dependent change in muscle properties.10aH-Reflex10amotor unit type10aoperant conditioning10aplasticity10atriceps surae1 aCarp, Jonathan, S.1 aChen, Xiang Yang1 aSheikh, H.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1168131402242nas a2200241   4500008004100000022001400041245008800055210006900143260001200212300001400224490000800238520154300246653002401789653001301813653001501826653001501841653001601856100002301872700002101895700001501916700002101931856004801952       2001                        eng d  a0014-481900aOperant conditioning of rat H-reflex affects motoneuron axonal conduction velocity.0 aOperant conditioning of rat Hreflex affects motoneuron axonal co  c01/2001  a269–2730 v1363 aThis study assessed the effects of operant conditioning of the H-reflex on motoneuron axonal conduction velocity in the rat. After measurement of the control H-reflex size, rats were either exposed for at least 40 days to the HRup or HRdown conditioning mode, in which reward occurred only if the soleus H-reflex was greater than (HRup mode) or less than (HRdown mode) a criterion or continued under the control condition (HRcon mode) in which the H-reflex was simply measured. We then measured axonal conduction velocity of triceps surae motor units of HRup, HRdown, and HRcon rats by stimulating the axon in the ventral root and recording from the tibial nerve. Conduction velocity was 8% less in successful HRdown rats than in HRcon rats (P=0.02). Conduction velocity in HRup rats and unsuccessful HRdown rats was not significantly different from that in HRcon rats. Since recording bypassed the intra-spinal portion of the motoneuron, the change was clearly in the axon. This decrease was similar to the 6% decrease previously found in successful HRdown monkeys. Unsuccessful HRdown rats and monkeys did not show this decrease. This result suggests that the mechanism of HRdown conditioning is similar in rats and monkeys and provides further support for the hypothesis that HRdown conditioning decreases motoneuron excitability by producing a positive shift in firing threshold. While traditional theories of learning emphasize synaptic plasticity, neuronal plasticity may also contribute to operantly conditioned behavioral changes.10aconduction velocity10aH-Reflex10amotoneuron10aplasticity10aSpinal Cord1 aCarp, Jonathan, S.1 aChen, Xiang Yang1 aSheikh, H.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1120629002143nas 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/1120629102520nas 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/900206101790nas a2200229   4500008004100000022001400041245005800055210005600113260001200169300001200181490000800193520117500201653001301376653002501389653001501414653000801429653001801437653001601455100002101471700002101492856004701513       1996                        eng d  a0014-481900aReversal of H-reflex operant conditioning in the rat.0 aReversal of Hreflex operant conditioning in the rat  c11/1996  a58–620 v1123 aIn response to an operant conditioning task, rats can gradually increase or decrease soleus H-reflex amplitude without change in background electromyographic activity or M response amplitude. Both increase (under the HRup mode) and decrease (under the HRdown mode) develop over weeks. The present study investigated reversal of conditioned H-reflex change. Following collection of control data, rats were exposed to one mode (HRup or HRdown) for 50 days, and then exposed to the opposite mode for up to 72 days. Rats responded to each mode exposure with gradual, mode-appropriate change in H-reflex amplitude. This finding is consistent with other evidence that H-reflex conditioning depends on spinal cord plasticity. The effects of exposure to the HRup (or HRdown) mode were not affected by whether exposure followed previous exposure to the HRdown (or HRup) mode. In accord with recent studies suggesting that HRup and HRdown conditioning have different spinal mechanisms, these results suggest that reversal of H-reflex change is due primarily to the superimposition of additional plasticity rather than to decay of the plasticity responsible for the initial change.10aH-Reflex10aoperant conditioning10aplasticity10arat10asoleus muscle10aSpinal Cord1 aChen, Xiang Yang1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/895140701682nas 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/747826201137nas a2200217   4500008004100000022001400041245003800055210003600093260001200129300001400141490000800155520059500163653002100758653001900779653001300798653000800811653001100819100002100830700002100851856004700872       1994                        eng d  a0006-899300aCircadian rhythm in rat H-reflex.0 aCircadian rhythm in rat Hreflex  c06/1994  a167–1700 v6483 aWe measured soleus H-reflex in the Sprague-Dawley rat as a function of time of day. H-reflex amplitude displayed a marked diurnal variation, even though background EMG and M-response amplitude were stable through the day. The H-reflex was largest in the late morning and smallest around midnight. Thus, its rhythm was opposite in phase to the circadian rhythm found in the primate H-reflex. This rhythm is a potentially confounding factor in studies of motor function. Furthermore, its existence implies that the CNS activity underlying a specific motor performance varies with time of day.10acircadian rhythm10aelectromyogram10aH-Reflex10arat10asoleus1 aChen, Xiang Yang1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/7922520