@article {3095,
	title = {H-reflex up-conditioning encourages recovery of EMG activity and H-reflexes after sciatic nerve transection and repair in rats.},
	journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
	volume = {30},
	year = {2010},
	month = {12/2010},
	pages = {16128{\textendash}16136},
	abstract = {Operant 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.},
	keywords = {conditioning, peripheral nerve, plasticity, Reflex, regeneration, Spinal Cord},
	issn = {1529-2401},
	doi = {10.1523/JNEUROSCI.4578-10.2010},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/21123559},
	author = {Yi Chen and Wang, Yu and Lu Chen and Sun, Chenyou and English, Arthur W. and Jonathan Wolpaw and Xiang Yang Chen}
}
@article {3210,
	title = {Spinal cord plasticity in acquisition and maintenance of motor skills.},
	journal = {Acta physiologica (Oxford, England)},
	volume = {189},
	year = {2007},
	month = {02/2007},
	pages = {155{\textendash}169},
	abstract = {Throughout 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{\textquoteright}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.},
	keywords = {conditioning, H-Reflex, Learning, Memory, motor function, plasticity, Rehabilitation, spinal cord injury},
	issn = {1748-1708},
	doi = {10.1111/j.1748-1716.2006.01656.x},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/17250566},
	author = {Jonathan Wolpaw}
}
@article {3211,
	title = {The education and re-education of the spinal cord.},
	journal = {Progress in brain research},
	volume = {157},
	year = {2006},
	month = {02/2006},
	pages = {261{\textendash}280},
	abstract = {In 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.},
	keywords = {behavior, conditioning, Learning, Memory, plasticity, Spinal Cord, spinal cord injury},
	issn = {0079-6123},
	doi = {10.1016/S0079-6123(06)57017-7},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/17167916},
	author = {Jonathan Wolpaw}
}
@article {3229,
	title = {Activity-dependent spinal cord plasticity in health and disease.},
	journal = {Annual review of neuroscience},
	volume = {24},
	year = {2001},
	month = {03/2001},
	pages = {807{\textendash}843},
	abstract = {Activity-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.},
	keywords = {behavior, conditioning, Learning, Memory, Rehabilitation, spinal cord injury},
	issn = {0147-006X},
	doi = {10.1146/annurev.neuro.24.1.807},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/11520919},
	author = {Jonathan Wolpaw and Tennissen, A. M.}
}
@article {3233,
	title = {Operant conditioning of rat H-reflex: effects on mean latency and duration.},
	journal = {Experimental brain research. Experimentelle Hirnforschung. Exp{\'e}rimentation c{\'e}r{\'e}brale},
	volume = {136},
	year = {2001},
	month = {01/2001},
	pages = {274{\textendash}279},
	abstract = {We 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.},
	keywords = {conditioning, H-Reflex, Memory, plasticity, Spinal Cord},
	issn = {0014-4819},
	doi = {10.1007/s002210000609},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/11206291},
	author = {Jonathan Wolpaw and Xiang Yang Chen}
}
@article {3231,
	title = {Time course of H-reflex conditioning in the rat.},
	journal = {Neuroscience letters},
	volume = {302},
	year = {2001},
	month = {04/2001},
	pages = {85{\textendash}88},
	abstract = {This 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.},
	keywords = {conditioning, Learning, Memory, plasticity, rat, Reflex, Spinal Cord},
	issn = {0304-3940},
	doi = {10.1016/S0304-3940(01)01658-5},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/11290393},
	author = {Xiang Yang Chen and Lu Chen and Jonathan Wolpaw}
}
@article {3241,
	title = {EEG-based communication: analysis of concurrent EMG activity.},
	journal = {Electroencephalography and clinical neurophysiology},
	volume = {107},
	year = {1998},
	month = {12/1998},
	pages = {428{\textendash}433},
	abstract = {OBJECTIVE:
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.},
	keywords = {augmentative communication, conditioning, Electroencephalography, Electromyography, mu rhythm, Rehabilitation, sensorimotor cortex},
	issn = {0013-4694},
	doi = {10.1016/S0013-4694(98)00107-2},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/9922089},
	author = {Theresa M Vaughan and Miner, L. A. and Dennis J. McFarland and Jonathan Wolpaw}
}
@article {3258,
	title = {Acquisition and maintenance of the simplest motor skill: investigation of CNS mechanisms.},
	journal = {Medicine and science in sports and exercise},
	volume = {26},
	year = {1994},
	month = {12/1994},
	pages = {1475{\textendash}1479},
	abstract = {The 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.},
	keywords = {conditioning, Learning, Memory, Motor control, plasticity, primate, Spinal Cord, training},
	issn = {0195-9131},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/7869882},
	author = {Jonathan Wolpaw}
}
@article {3171,
	title = {The volitional nature of the simplest reflex.},
	journal = {Acta neurobiologiae experimentalis},
	volume = {53},
	year = {1993},
	pages = {103{\textendash}111},
	abstract = {Recent 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.},
	keywords = {behavior, Brain, conditioning, human physiology, Learning, Memory, motoneuron, nature, primate, Reflex, Spinal Cord, spinal site, supra spinal site, vertebrate},
	issn = {0065-1400},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/8317238},
	author = {Jonathan Wolpaw and Jonathan S. Carp}
}
@article {3269,
	title = {Operant conditioning of H-reflex in freely moving monkeys.},
	journal = {Journal of neuroscience methods},
	volume = {31},
	year = {1990},
	month = {02/1990},
	pages = {145{\textendash}152},
	abstract = {The 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.},
	keywords = {conditioning, H-Reflex, Memory, plasticity, primate, spinal reflex, stretch reflex},
	issn = {0165-0270},
	doi = {10.1016/0165-0270(90)90159-D},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/2319815},
	author = {Jonathan Wolpaw and Herchenroder, P. A.}
}
@article {3178,
	title = {Memory traces in spinal cord produced by H-reflex conditioning: effects of post-tetanic potentiation.},
	journal = {Neuroscience letters},
	volume = {103},
	year = {1989},
	month = {08/1989},
	pages = {113{\textendash}119},
	abstract = {Operant 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.},
	keywords = {conditioning, Learning, Memory, motoneuron, potentiation, primate, spinal reflex},
	issn = {0304-3940},
	doi = {10.1016/0304-3940(89)90495-3},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/2779852},
	author = {Jonathan Wolpaw and Jonathan S. Carp and Lee, C. L.}
}
