02599nas 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/2112355902003nas a2200241   4500008004100000022001400041245007500055210006900130260001200199300001400211490000800225520132900233653001701562653001301579653001301592653001101605653001901616653001501635653001901650653002301669100002101692856004801713       2007                        eng d  a1748-170800aSpinal cord plasticity in acquisition and maintenance of motor skills.0 aSpinal cord plasticity in acquisition and maintenance of motor s  c02/2007  a155–1690 v1893 aThroughout normal life, activity-dependent plasticity occurs in the spinal cord as well as in brain. Like other central nervous system (CNS) plasticity, spinal cord plasticity can occur at numerous neuronal and synaptic sites and through a variety of mechanisms. Spinal cord plasticity is prominent early in life and contributes to mastery of standard behaviours like locomotion and rapid withdrawal from pain. Later in life, spinal cord plasticity has a role in acquisition and maintenance of new motor skills, and in compensation for peripheral and central changes accompanying ageing, disease and trauma. Mastery of the simplest behaviours is accompanied by complex spinal and supraspinal plasticity. This complexity is necessary, in order to preserve the complete behavioural repertoire, and is also inevitable, due to the ubiquity of activity-dependent CNS plasticity. Explorations of spinal cord plasticity are necessary for understanding motor skills. Furthermore, the spinal cord's comparative simplicity and accessibility makes it a logical starting point for studying skill acquisition. Induction and guidance of activity-dependent spinal cord plasticity will probably play an important role in realization of effective new rehabilitation methods for spinal cord injuries, cerebral palsy and other motor disorders.10aconditioning10aH-Reflex10aLearning10aMemory10amotor function10aplasticity10aRehabilitation10aspinal cord injury1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1725056601977nas a2200229   4500008004100000022001400041245005500055210004900110260001200159300001400171490000800185520137700193653001301570653001701583653001301600653001101613653001501624653001601639653002301655100002101678856004801699       2006                        eng d  a0079-612300aThe education and re-education of the spinal cord.0 aeducation and reeducation of the spinal cord  c02/2006  a261–2800 v1573 aIn normal life, activity-dependent plasticity occurs in the spinal cord as well as in the brain. Like CNS plasticity elsewhere, this spinal cord plasticity can occur at many neuronal and synaptic sites and by a variety of mechanisms. Spinal cord plasticity is prominent in postnatal development and contributes to acquisition of standard behaviors such as locomotion and rapid withdrawal from pain. Later on in life, spinal cord plasticity contributes to acquisition and maintenance of specialized motor skills, and to compensation for the peripheral and central changes associated with aging, disease, and trauma. Mastery of even the simplest behaviors is accompanied by complex spinal and supraspinal plasticity. This complexity is necessary, to preserve the full roster of behaviors, and is also inevitable, due to the ubiquity of activity-dependent plasticity in the CNS. Careful investigation of spinal cord plasticity is essential for understanding motor skills; and, because of the relative simplicity and accessibility of the spinal cord, is a logical and convenient starting point for exploring skill acquisition. Appropriate induction and guidance of activity-dependent plasticity in the spinal cord is likely to be a key part of the realization of effective new rehabilitation methods for spinal cord injuries, cerebral palsy, and other chronic motor disorders.10abehavior10aconditioning10aLearning10aMemory10aplasticity10aSpinal Cord10aspinal cord injury1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1716791603278nas a2200229   4500008004100000022001400041245006900055210006700124260001200191300001400203490000700217520263700224653001302861653001702874653001302891653001102904653001902915653002302934100002102957700002202978856004803000       2001                        eng d  a0147-006X00aActivity-dependent spinal cord plasticity in health and disease.0 aActivitydependent spinal cord plasticity in health and disease  c03/2001  a807–8430 v243 aActivity-dependent plasticity occurs in the spinal cord throughout life. Driven by input from the periphery and the brain, this plasticity plays an important role in the acquisition and maintenance of motor skills and in the effects of spinal cord injury and other central nervous system disorders. The responses of the isolated spinal cord to sensory input display sensitization, long-term potentiation, and related phenomena that contribute to chronic pain syndromes; they can also be modified by both classical and operant conditioning protocols. In animals with transected spinal cords and in humans with spinal cord injuries, treadmill training gradually modifies the spinal cord so as to improve performance. These adaptations by the isolated spinal cord are specific to the training regimen and underlie new approaches to restoring function after spinal cord injury. Descending inputs from the brain that occur during normal development, as a result of supraspinal trauma, and during skill acquisition change the spinal cord. The early development of adult spinal cord reflex patterns is driven by descending activity; disorders that disrupt descending activity later in life gradually change spinal cord reflexes. Athletic training, such as that undertaken by ballet dancers, is associated with gradual alterations in spinal reflexes that appear to contribute to skill acquisition. Operant conditioning protocols in animals and humans can produce comparable reflex changes and are associated with functional and structural plasticity in the spinal cord, including changes in motoneuron firing threshold and axonal conduction velocity, and in synaptic terminals on motoneurons. The corticospinal tract has a key role in producing this plasticity. Behavioral changes produced by practice or injury reflect the combination of plasticity at multiple spinal cord and supraspinal sites. Plasticity at multiple sites is both necessary-to insure continued performance of previously acquired behaviors-and inevitable-due to the ubiquity of the capacity for activity-dependent plasticity in the central nervous system. Appropriate induction and guidance of activity-dependent plasticity in the spinal cord is an essential component of new therapeutic approaches aimed at maximizing function after spinal cord injury or restoring function to a newly regenerated spinal cord. Because plasticity in the spinal cord contributes to skill acquisition and because the spinal cord is relatively simple and accessible, this plasticity is a logical and practical starting point for studying the acquisition and maintenance of skilled behaviors.10abehavior10aconditioning10aLearning10aMemory10aRehabilitation10aspinal cord injury1 aWolpaw, Jonathan1 aTennissen, A., M.  uhttp://www.ncbi.nlm.nih.gov/pubmed/1152091902143nas a2200217   4500008004100000022001400041245008000055210006900135260001200204300001400216490000800230520152500238653001701763653001301780653001101793653001501804653001601819100002101835700002101856856004801877       2001                        eng d  a0014-481900aOperant conditioning of rat H-reflex: effects on mean latency and duration.0 aOperant conditioning of rat Hreflex effects on mean latency and   c01/2001  a274–2790 v1363 aWe are currently studying the mechanisms of operantly conditioned changes in the H-reflex in the rat. Primate data suggest that H-reflex decrease is due to a positive shift in motoneuron firing threshold and a small decrease in the monosynaptic excitatory postsynaptic potential (EPSP), and that increase might be due to change in group-I oligosynaptic (especially disynaptic) input. To further evaluate the possibility of conditioned change in oligosynaptic input, we compared the mean latency (i.e., the average latency of the entire H-reflex) and the duration of control (i.e., pre-conditioning) H-reflexes with those of H-reflexes after up-conditioning or down-conditioning. Up-conditioning was associated with small, statistically significant increases in H-reflex mean latency [+0.11+/-0.05 (+/-SE) ms] and duration (+0.32+/-0.16 ms). The mean latency of the H-reflex increase (i.e., the part added to the H-reflex by up-conditioning) was 0.28+/-0.14 (+/-SE) ms greater than that of the control H-reflex. Down-conditioning had no significant effect on mean latency or duration. While these results indicate that operant conditioning does not greatly change H-reflex mean latency or duration, the effects detected with up-conditioning are consistent with the hypothesis that decreased inhibition, or increased excitation, by homonymous and heteronymous group-I oligosynaptic input contributes to the H-reflex increase produced by up-conditioning. Several other mechanisms might also account for these small effects.10aconditioning10aH-Reflex10aMemory10aplasticity10aSpinal Cord1 aWolpaw, Jonathan1 aChen, Xiang Yang  uhttp://www.ncbi.nlm.nih.gov/pubmed/1120629101999nas a2200253   4500008004100000022001400041245005300055210005100108260001200159300001200171490000800183520136000191653001701551653001301568653001101581653001501592653000801607653001101615653001601626100002101642700001301663700002101676856004801697       2001                        eng d  a0304-394000aTime course of H-reflex conditioning in the rat.0 aTime course of Hreflex conditioning in the rat  c04/2001  a85–880 v3023 aThis study sought to define the course of operantly conditioned change in the rat soleus H-reflex and to determine whether, like H-reflex conditioning and spinal stretch reflex conditioning in the monkey, it develops in distinct phases. Data from 33 rats in which the right soleus H-reflex was trained up (i.e. HRup mode) and 38 in which it was trained down (i.e. HRdown mode) were averaged to define the courses of H-reflex increase and decrease. In HRup rats, the H-reflex showed a large phase I increase within the first 2 days followed by gradual phase II increase that continued for weeks. In HRdown rats, the H-reflex appeared to show a small phase I decrease and then showed a gradual phase II decrease over weeks. In combination with other recent work, the data suggest that H-reflex conditioning begins with a rapid mode-appropriate alteration in corticospinal tract influence over the spinal arc of the H-reflex, which causes phase I change, and that the continuation of this altered influence induces gradual spinal cord plasticity that is responsible for phase II change. The results further establish the similarity of H-reflex conditioning in primates and rats. Thus, they encourage efforts to produce a single coherent model of the phenomenon based on data from the two species and indicate the potential clinical relevance of the rat data.10aconditioning10aLearning10aMemory10aplasticity10arat10aReflex10aSpinal Cord1 aChen, Xiang Yang1 aChen, Lu1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/1129039302088nas a2200265   4500008004100000022001400041245006600055210006300121260001200184300001400196490000800210520131500218653003101533653001701564653002701581653002101608653001401629653001901643653002401662100002401686700001801710700002601728700002101754856004701775       1998                        eng d  a0013-469400aEEG-based communication: analysis of concurrent EMG activity.0 aEEGbased communication analysis of concurrent EMG activity  c12/1998  a428–4330 v1073 aOBJECTIVE:
Recent studies indicate that people can learn to control the amplitude of mu or beta rhythms in the EEG recorded from the scalp over sensorimotor cortex and can use that control to move a cursor to targets on the computer screen. While subjects do not move during performance, it is possible that inapparent or unconscious muscle contractions contribute to the changes in the mu and beta rhythm activity responsible for cursor movement. We evaluated this possibility.
METHODS:
EMG was recorded from 10 distal limb muscle groups while five trained subjects used mu or beta rhythms to move a cursor to targets at the bottom or top edge of a computer screen.
RESULTS:
EMG activity was very low during performance, averaging 4.0+/-4.4% (SD) of maximum voluntary contraction. Most important, the correlation, measured as r2, between target position and EMG activity averaged only 0.01+/-0.02, much lower than the correlation between target position and the EEG activity that controlled cursor movement, which averaged 0.39+/-0.18.
CONCLUSIONS:
These results strongly support the conclusion that EEG-based cursor control does no depend on concurrent muscle activity. EEG-based communication and control might provide a new augmentative communication option for those with severe motor disabilities.10aaugmentative communication10aconditioning10aElectroencephalography10aElectromyography10amu rhythm10aRehabilitation10asensorimotor cortex1 aVaughan, Theresa, M1 aMiner, L., A.1 aMcFarland, Dennis, J.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/992208902070nas a2200241   4500008004100000022001400041245009400055210006900149260001200218300001600230490000700246520139200253653001701645653001301662653001101675653001801686653001501704653001201719653001601731653001301747100002101760856004701781       1994                        eng d  a0195-913100aAcquisition and maintenance of the simplest motor skill: investigation of CNS mechanisms.0 aAcquisition and maintenance of the simplest motor skill investig  c12/1994  a1475–14790 v263 aThe spinal stretch reflex (SSR), or tendon jerk, is the simplest behavior of the vertebrate nervous system. It is mediated primarily by a wholly spinal, two-neuron pathway. Recent studies from several laboratories have shown that primates, human and nonhuman, can gradually increase or decrease the size of the SSR when reward depends on such change. Evidence of this training remains in the spinal cord after all supraspinal influence is removed. Thus, the learning of this simple motor skill changes the spinal cord itself. Comparable spinal plasticity probably plays a role in the acquisition of many complex motor skills. Intracellular physiological and anatomical studies are seeking the location and nature of this spinal cord plasticity. Attention focuses on the most probable sites of change, the group Ia afferent synapse on the alpha motoneuron and the motoneuron itself. Results to date indicate that modifications are present at several places in the spinal cord. Current clinical studies are investigating the use of spinal cord adaptive plasticity as a basis for a new therapeutic approach to spasticity and other forms of abnormal spinal reflex function that result from spinal cord injury, stroke, or other neurological disorders. In the future, understanding of spinal reflex plasticity may lead to development of improved training methods for a variety of motor skills.10aconditioning10aLearning10aMemory10aMotor control10aplasticity10aprimate10aSpinal Cord10atraining1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/786988201213nas a2200313   4500008004100000022001400041245005000055210004500105300001400150490000700164520043400171653001300605653001000618653001700628653002100645653001300666653001100679653001500690653001100705653001200716653001100728653001600739653001600755653002200771653001500793100002100808700002300829856004700852       1993                        eng d  a0065-140000aThe volitional nature of the simplest reflex.0 avolitional nature of the simplest reflex  a103–1110 v533 aRecent studies suggest that none of the behaviors of the vertebrate CNS are fixed responses incapable of change. Even the simplest reflex of all, the two-neuron, monosynaptic spinal stretch reflex (SSR), undergoes adaptive change under appropriate circumstances. Operantly conditioned SSR change occurs gradually over days and weeks and is associated with a complex pattern of CNS plasticity at both spinal and supraspinal sites.10abehavior10aBrain10aconditioning10ahuman physiology10aLearning10aMemory10amotoneuron10anature10aprimate10aReflex10aSpinal Cord10aspinal site10asupra spinal site10avertebrate1 aWolpaw, Jonathan1 aCarp, Jonathan, S.  uhttp://www.ncbi.nlm.nih.gov/pubmed/831723801398nas a2200241   4500008004100000022001400041245006300055210006100118260001200179300001400191490000700205520074600212653001700958653001300975653001100988653001500999653001201014653001801026653001901044100002101063700002501084856004701109       1990                        eng d  a0165-027000aOperant conditioning of H-reflex in freely moving monkeys.0 aOperant conditioning of Hreflex in freely moving monkeys  c02/1990  a145–1520 v313 aThe H-reflex, the electrical analog of the stretch reflex or tendon jerk, is the simplest behavior of the primate CNS. It is subserved by a wholly spinal two-neuron reflex arc. Recent studies show that this reflex can be increased or decreased by operant conditioning, and that such conditioning causes plastic changes in the spinal cord itself. Thus, H-reflex conditioning provides a powerful new model for investigating primate memory traces. The key feature of this model, the conditioning task, originally required animal restraint. This report describes a new tether-based design that allows H-reflex measurement and conditioning without restraint. This design integrates the conditioning task into the life of the freely moving animal.10aconditioning10aH-Reflex10aMemory10aplasticity10aprimate10aspinal reflex10astretch reflex1 aWolpaw, Jonathan1 aHerchenroder, P., A.  uhttp://www.ncbi.nlm.nih.gov/pubmed/231981501769nas a2200253   4500008004100000022001400041245010600055210006900161260001200230300001400242490000800256520104100264653001701305653001301322653001101335653001501346653001701361653001201378653001801390100002101408700002301429700001601452856004701468       1989                        eng d  a0304-394000aMemory traces in spinal cord produced by H-reflex conditioning: effects of post-tetanic potentiation.0 aMemory traces in spinal cord produced by Hreflex conditioning ef  c08/1989  a113–1190 v1033 aOperant conditioning of the wholly spinal, largely monosynaptic triceps surae H-reflex in monkeys causes changes in lumbosacral spinal cord that persist after removal of supraspinal influence. We evaluated the interaction between post-tetanic potentiation and these memory traces. Animals in which the triceps surae H-reflex in one leg had been increased or decreased by conditioning were deeply anesthetized, and monosynaptic reflexes to L6-S1 dorsal root stimulation were recorded before and after tetanization from both legs for 3 days after thoracic cord transection. Animals remained anesthetized throughout and were sacrificed by overdose. Reflex asymmetries consistent with the effect of H-reflex conditioning were present after transection and persisted through the 3 days of study. Tetanization affected conditioned leg and control leg reflexes similarly. This finding suggests that, while post-tetanic potentiation and probably H-reflex conditioning alter Ia synaptic transmission, the two phenomena have different mechanisms.10aconditioning10aLearning10aMemory10amotoneuron10apotentiation10aprimate10aspinal reflex1 aWolpaw, Jonathan1 aCarp, Jonathan, S.1 aLee, C., L.  uhttp://www.ncbi.nlm.nih.gov/pubmed/2779852