01870nas a2200265   4500008004100000022001400041245008400055210006900139260001200208300001200220490000700232520108800239653002501327653001301352653002701365653002501392653001501417653001901432653001801451100001601469700001601485700001801501700002101519856006401540       2018                        eng d  a1878-747900aRetraining Reflexes: Clinical Translation of Spinal Reflex Operant Conditioning0 aRetraining Reflexes Clinical Translation of Spinal Reflex Operan  c07/2018  a669-6830 v153 aNeurological disorders, such as spinal cord injury, stroke, traumatic brain injury, cerebral palsy, and multiple sclerosis cause motor impairments that are a huge burden at the individual, family, and societal levels. Spinal reflex abnormalities contribute to these impairments. Spinal reflex measurements play important roles in characterizing and monitoring neurological disorders and their associated motor impairments, such as spasticity, which affects nearly half of those with neurological disorders. Spinal reflexes can also serve as therapeutic targets themselves. Operant conditioning protocols can target beneficial plasticity to key reflex pathways; they can thereby trigger wider plasticity that improves impaired motor skills, such as locomotion. These protocols may complement standard therapies such as locomotor training and enhance functional recovery. This paper reviews the value of spinal reflexes and the therapeutic promise of spinal reflex operant conditioning protocols; it also considers the complex process of translating this promise into clinical reality.10aclinical translation10aH-Reflex10aneurological disorders10aoperant conditioning10aplasticity10aRehabilitation10aspinal reflex1 aEftekhar, A1 aNorton, JJS1 aMcDonough, CM1 aWolpaw, Jonathan  uhttps://link.springer.com/article/10.1007/s13311-018-0643-202131nas a2200253   4500008004100000245007200041210006900113260000900182300001400191490000700205520141800212653001301630653001901643653002501662653001501687653001901702653001601721100001301737700001301750700001301763700002201776700002101798856005801819       2017                        eng d00aWhy New Spinal Cord Plasticity Does Not Disrupt Old Motor Behaviors0 aWhy New Spinal Cord Plasticity Does Not Disrupt Old Motor Behavi  cJuly  a8198-82060 v373 aWhen new motor learning changes the spinal cord, old behaviors are not impaired; their key features are preserved by additional compensatory plasticity. To explore the mechanisms responsible for this compensatory plasticity, we transected the spinal dorsal ascending tract before or after female rats acquired a new behavior—operantly conditioned increase or decrease in the right soleus H-reflex—and examined an old behavior—locomotion. Neither spinal dorsal ascending tract transection nor H-reflex conditioning alone impaired locomotion. Nevertheless, when spinal dorsal ascending tract transection and H-reflex conditioning were combined, the rats developed a limp and a tilted posture that correlated in direction and magnitude with the H-reflex change. When the right H-reflex was increased by conditioning, the right step lasted longer than the left and the right hip was higher than the left; when the right H-reflex was decreased by conditioning, the opposite occurred. These results indicate that ascending sensory input guides the compensatory plasticity that normally prevents the plasticity underlying H-reflex change from impairing locomotion. They support the concept of the state of the spinal cord as a negotiated equilibrium that reflects the concurrent influences of all the behaviors in an individual's repertoire; and they support the new therapeutic strategies this concept introduces.10aH-Reflex10amotor learning10aoperant conditioning10aplasticity10aRehabilitation10aSpinal Cord1 aChen, Yi1 aChen, Lu1 aWang, Yu1 aChen, Xiang, Yang1 aWolpaw, Jonathan  uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5566867/02554nas a2200241   4500008004100000022001400041245016400055210006900219260001200288300001200300490000800312520178000320653001302100653001502113653001902128653001602147653001502163100002102178700002202199700002102221700002202242856004802264       2014                        eng d  a1522-159800aOperant conditioning of the soleus H-reflex does not induce long-term changes in the gastrocnemius H-reflexes and does not disturb normal locomotion in humans.0 aOperant conditioning of the soleus Hreflex does not induce longt  c09/2014  a1439-460 v1123 a<p>In normal animals, operant conditioning of the spinal stretch reflex or the H-reflex has lesser effects on synergist muscle reflexes. In rats and people with incomplete spinal cord injury (SCI), soleus H-reflex operant conditioning can improve locomotion. We studied in normal humans the impact of soleus H-reflex down-conditioning on medial (MG) and lateral gastrocnemius (LG) H-reflexes and on locomotion. Subjects completed 6 baseline and 30 conditioning sessions. During conditioning trials, the subject was encouraged to decrease soleus H-reflex size with the aid of visual feedback. Every sixth session, MG and LG H-reflexes were measured. Locomotion was assessed before and after conditioning. In successfully conditioned subjects, the soleus H-reflex decreased 27.2%. This was the sum of within-session (task dependent) adaptation (13.2%) and across-session (long term) change (14%). The MG H-reflex decreased 14.5%, due mainly to task-dependent adaptation (13.4%). The LG H-reflex showed no task-dependent adaptation or long-term change. No consistent changes were detected across subjects in locomotor H-reflexes, EMG activity, joint angles, or step symmetry. Thus, in normal humans, soleus H-reflex down-conditioning does not induce long-term changes in MG/LG H-reflexes and does not change locomotion. In these subjects, task-dependent adaptation of the soleus H-reflex is greater than it is in people with SCI, whereas long-term change is less. This difference from results in people with SCI is consistent with the fact that long-term change is beneficial in people with SCI, since it improves locomotion. In contrast, in normal subjects, long-term change is not beneficial and may necessitate compensatory plasticity to preserve satisfactory locomotion.</p>10aLearning10aplasticity10aRehabilitation10aSpinal Cord10asynergists1 aMakihara, Yukiko1 aSegal, Richard, L1 aWolpaw, Jonathan1 aThompson, Aiko, K  uhttp://www.ncbi.nlm.nih.gov/pubmed/2494421602449nas a2200241   4500008004100000022001400041245010300055210006900158260001200227300001600239490000700255520172600262653001301988653001502001653002502016653001502041653001902056653001502075100002302090700002502113700002102138856004802159       2013                        eng d  a1529-240100aOperant conditioning of a spinal reflex can improve locomotion after spinal cord injury in humans.0 aOperant conditioning of a spinal reflex can improve locomotion a  c02/2013  a2365–23750 v333 aOperant conditioning protocols can modify the activity of specific spinal cord pathways and can thereby affect behaviors that use these pathways. To explore the therapeutic application of these protocols, we studied the impact of down-conditioning the soleus H-reflex in people with impaired locomotion caused by chronic incomplete spinal cord injury. After a baseline period in which soleus H-reflex size was measured and locomotion was assessed, subjects completed either 30 H-reflex down-conditioning sessions (DC subjects) or 30 sessions in which the H-reflex was simply measured [unconditioned (UC) subjects], and locomotion was reassessed. Over the 30 sessions, the soleus H-reflex decreased in two-thirds of the DC subjects (a success rate similar to that in normal subjects) and remained smaller several months later. In these subjects, locomotion became faster and more symmetrical, and the modulation of EMG activity across the step cycle increased bilaterally. Furthermore, beginning about halfway through the conditioning sessions, all of these subjects commented spontaneously that they were walking faster and farther in their daily lives, and several noted less clonus, easier stepping, and/or other improvements. The H-reflex did not decrease in the other DC subjects or in any of the UC subjects; and their locomotion did not improve. These results suggest that reflex-conditioning protocols can enhance recovery of function after incomplete spinal cord injuries and possibly in other disorders as well. Because they are able to target specific spinal pathways, these protocols could be designed to address each individual's particular deficits, and might thereby complement other rehabilitation methods.10aLearning10aLocomotion10aoperant conditioning10aplasticity10aRehabilitation10aspasticity1 aThompson, Aiko, K.1 aPomerantz, Ferne, R.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/2339266601657nas a2200217   4500008004100000022001400041245008100055210006900136260001200205300001400217490000700231520101900238653001901257653001501276653001901291653001601310100002301326700002101349700002101370856004801391       2013                        eng d  a1097-459800aSoleus H-reflex operant conditioning changes the H-reflex recruitment curve.0 aSoleus Hreflex operant conditioning changes the Hreflex recruitm  c04/2013  a539–5440 v473 aINTRODUCTION:
Operant conditioning can gradually change the human soleus H-reflex. The protocol conditions the reflex near M-wave threshold. In this study we examine its impact on the reflexes at other stimulus strengths.
METHODS:
H-reflex recruitment curves were obtained before and after a 24-session exposure to an up-conditioning (HRup) or a down-conditioning (HRdown) protocol and were compared.
RESULTS:
In both HRup and HRdown subjects, conditioning affected the entire H-reflex recruitment curve. In 5 of 6 HRup and 3 of 6 HRdown subjects, conditioning elevated (HRup) or depressed (HRdown), respectively, the entire curve. In the other HRup subject or the other 3 HRdown subjects, the curve was shifted to the left or to the right, respectively.
CONCLUSIONS:
H-reflex conditioning does not simply change the H-reflex to a stimulus of particular strength; it also changes the H-reflexes to stimuli of different strengths. Thus, it is likely to affect many actions in which this pathway participates.10amotor learning10aplasticity10aRehabilitation10aSpinal Cord1 aThompson, Aiko, K.1 aChen, Xiang Yang1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/2328110702599nas a2200289   4500008004100000022001400041245013200055210006900187260001200256300001800268490000700286520174900293653001702042653002102059653001502080653001102095653001702106653001602123100001302139700001302152700001302165700001702178700002402195700002102219700002102240856004802261       2010                        eng d  a1529-240100aH-reflex up-conditioning encourages recovery of EMG activity and H-reflexes after sciatic nerve transection and repair in rats.0 aHreflex upconditioning encourages recovery of EMG activity and H  c12/2010  a16128–161360 v303 aOperant conditioning of the spinal stretch reflex or its electrical analog, the H-reflex, produces spinal cord plasticity and can thereby affect motoneuron responses to primary afferent input. To explore whether this conditioning can affect the functional outcome after peripheral nerve injury, we assessed the effect of up-conditioning soleus (SOL) H-reflex on SOL and tibialis anterior (TA) function after sciatic nerve transection and repair. Sprague Dawley rats were implanted with EMG electrodes in SOL and TA and stimulating cuffs on the posterior tibial nerve. After control data collection, the sciatic nerve was transected and repaired and the rat was exposed for 120 d to continued control data collection (TC rats) or SOL H-reflex up-conditioning (TU rats). At the end of data collection, motoneurons that had reinnervated SOL and TA were labeled retrogradely. Putative primary afferent terminals [i.e., terminals containing vesicular glutamate transporter-1 (VGLUT1)] on SOL motoneurons were studied immunohistochemically. SOL (and probably TA) background EMG activity recovered faster in TU rats than in TC rats, and the final recovered SOL H-reflex was significantly larger in TU than in TC rats. TU and TC rats had significantly fewer labeled motoneurons and higher proportions of double-labeled motoneurons than untransected rats. VGLUT1 terminals were significantly more numerous on SOL motoneurons of TU than TC rats. Combined with the larger H-reflexes in TU rats, this anatomical finding supports the hypothesis that SOL H-reflex up-conditioning strengthened primary afferent reinnervation of SOL motoneurons. These results suggest that H-reflex up-conditioning may improve functional recovery after nerve injury and repair.10aconditioning10aperipheral nerve10aplasticity10aReflex10aregeneration10aSpinal Cord1 aChen, Yi1 aWang, Yu1 aChen, Lu1 aSun, Chenyou1 aEnglish, Arthur, W.1 aWolpaw, Jonathan1 aChen, Xiang Yang  uhttp://www.ncbi.nlm.nih.gov/pubmed/2112355901519nas 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/1942024602003nas 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/1716791602190nas 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/1664718102878nas 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/1197676202272nas 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/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/1129039302520nas 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/1009896201573nas 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/941667302267nas 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/895140702070nas 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/786988202325nas a2200229   4500008004100000022001400041245009300055210006900148260001200217300001200229490000700241520165100248653001301899653001101912653002501923653001501948653001601963100002101979700002502000700002302025856004702048       1993                        eng d  a0014-481900aOperant conditioning of the primate H-reflex: factors affecting the magnitude of change.0 aOperant conditioning of the primate Hreflex factors affecting th  c12/1993  a31–390 v973 aPrimates can gradually increase or decrease H-reflex amplitude in one leg when reward depends on that amplitude. The magnitude of change varies greatly from animal to animal. This study sought to define the factors that control this magnitude. It evaluated the influence of animal age, muscle size (absolute and relative), background electromyographic activity (EMG) level, M response amplitude, initial H-reflex amplitude, performance intensity, and behavior of the contralateral leg. Fifty-four animals (Macaca nemestrina) underwent operant conditioning of the triceps surae H-reflex in one leg (the trained leg). Twenty-eight were rewarded for larger H-reflexes (HRup animals), and 26 were rewarded for smaller H-reflexes (HRdown animals). In the HRup animals, H-reflex amplitude in the trained leg rose to an average final value of 177% of its initial amplitude. Magnitude of increase varied widely across animals. Nine animals rose to 120-140%, 11 to 160-240%, three to 300% or more, and five remained within 20% of initial amplitude. In the HRdown animals, H-reflex amplitude in the trained leg decreased to an average of 69% of initial amplitude. Magnitude of decrease varied widely. Five animals decreased to 20-40%, seven to 40-60%, six to 60-80%, and eight remained within 20% of initial amplitude. Animal age, as assessed by weight, markedly affected HRdown conditioning, but not HRup conditioning. Heavy HRdown animals (> or = 6 kg) were more successful than light HRdown animals (< 6 kg). Thirteen of 14 heavy animals and only five of 12 light animals decreased to less than 80% of initial amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)10aH-Reflex10amonkey10aoperant conditioning10aplasticity10aSpinal Cord1 aWolpaw, Jonathan1 aHerchenroder, P., A.1 aCarp, Jonathan, S.  uhttp://www.ncbi.nlm.nih.gov/pubmed/813183001398nas 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/231981501794nas 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/399105701504nas 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