Early spread of hyperexcitability to caudal dorsal horn networks after a chemically-induced lesion of the rat spinal cord in vitro

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.

► Chemically-induced spinal lesion evokes wide-spread dorsal root depolarization. ► Dorsal horns remote from the spinal lesion show early hyperexcitability. ► Remote segments show the impaired expression of GABA synthetic enzyme.