Corticospinal tract transection permanently abolishes H-reflex down-conditioning in rats.

TitleCorticospinal tract transection permanently abolishes H-reflex down-conditioning in rats.
Publication TypeJournal Article
Year of Publication2006
AuthorsChen, XY, Chen, Y, Chen, L, Tennissen, AM, Wolpaw, J
JournalJournal of neurotrauma
Volume23
Pagination1705–1712
Date Published11/2006
ISSN0897-7151
Keywordscorticospinal tract, H-reflex conditioning, plasticity, rat, spinal cord injury
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.

URLhttp://www.ncbi.nlm.nih.gov/pubmed/17115915
DOI10.1089/neu.2006.23.1705

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