@article {4094,
	title = {Why New Spinal Cord Plasticity Does Not Disrupt Old Motor Behaviors},
	journal = {The Journal of Neuroscience},
	volume = {37},
	year = {2017},
	month = {July},
	pages = {8198-8206},
	abstract = {When 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{\textemdash}operantly conditioned increase or decrease in the right soleus H-reflex{\textemdash}and examined an old behavior{\textemdash}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{\textquoteright}s repertoire; and they support the new therapeutic strategies this concept introduces.},
	keywords = {H-Reflex, motor learning, operant conditioning, plasticity, Rehabilitation, Spinal Cord},
	doi = {10.1523/JNEUROSCI.0767-17.2017},
	url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5566867/},
	author = {Chen, Yi and Chen, Lu and Wang, Yu and Chen, Xiang Yang and Jonathan Wolpaw}
}
@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 {3100,
	title = {Reflex conditioning: a new strategy for improving motor function after spinal cord injury.},
	journal = {Annals of the New York Academy of Sciences},
	volume = {1198 Suppl 1},
	year = {2010},
	month = {06/2010},
	pages = {E12{\textendash}E21},
	abstract = {Spinal 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.},
	keywords = {H-Reflex, learning and memory, Locomotion, plasticity, reflex conditioning, Rehabilitation, spinal cord injury},
	issn = {1749-6632},
	doi = {10.1111/j.1749-6632.2010.05565.x},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/20590534},
	author = {Xiang Yang Chen and Yi Chen and Wang, Yu and Thompson, Aiko and Jonathan S. Carp and Segal, Richard L. and Jonathan Wolpaw}
}
