@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}
}
@article {3190,
	title = {Corticospinal tract transection permanently abolishes H-reflex down-conditioning in rats.},
	journal = {Journal of neurotrauma},
	volume = {23},
	year = {2006},
	month = {11/2006},
	pages = {1705{\textendash}1712},
	abstract = {Previous 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.},
	keywords = {corticospinal tract, H-reflex conditioning, plasticity, rat, spinal cord injury},
	issn = {0897-7151},
	doi = {10.1089/neu.2006.23.1705},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/17115915},
	author = {Xiang Yang Chen and Yi Chen and Lu Chen and Tennissen, Ann M. and Jonathan Wolpaw}
}
