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- R Deumens, G L Mazzone, and G Taccola.
- Institute of Neuroscience, Université catholique de Louvain, Brussels, Belgium. deumensr@gmail.com
- Neuroscience. 2013 Jan 15;229:155-63.
AbstractHyperexcitability 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.Copyright © 2012 IBRO. Published by Elsevier Ltd. All rights reserved.
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