title: Early spread of hyperexcitability to caudal dorsal horn networks after a chemically-induced lesion of the rat spinal cord in vitro.
abstract: Hyperexcitability of dorsal horn neurons has been shown to play a key role in neuropathic pain following chronic experimental spinal cord injury. With a neonatal in vitro spinal cord injury model, we show that a chemically-induced lesion leads to rapid gain-of-function of sublesional dorsal horn networks biased to hyperexcitation. The expression of the GABA synthetic enzyme GAD65 was significantly reduced at the same level of the spinal cord, suggesting a compromised inhibitory system. We propose that our model could be useful to test early approaches to contrast spinal cord injury-induced central sensitization of dorsal horn circuits.
authors.affiliation: Institute of Neuroscience, Université catholique de Louvain, Brussels, Belgium. deumensr@gmail.com
authors.forename: R
authors.initials: R
authors.lastname: Deumens
authors.forename: G L
authors.initials: GL
authors.lastname: Mazzone
authors.forename: G
authors.initials: G
authors.lastname: Taccola
mesh_terms: D000818:Animals; D005968:Glutamate Decarboxylase / Q000378:metabolism; D007608:Kainic Acid; D009437:Neuralgia / Q000378:metabolism / Q000503:physiopathology; D020671:Posterior Horn Cells / Q000378:metabolism / Q000503:physiopathology*; D051381:Rats; D013116:Spinal Cord / Q000378:metabolism / Q000503:physiopathology*; D013119:Spinal Cord Injuries / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2; D007608:Kainic Acid