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After axotomy, application of muscimol, a GABAAreceptor agonist, induced an increase in intracellular Ca2+([Ca2+]i) in dorsal motor neurons of the vagus (DMV neurons). Elevation of [Ca2+]i by muscimol was blocked by bicuculline, tetrodotoxin, and Ni2+. In axotomized DMV neurons measured with gramicidin perforated-patch recordings, reversal potentials of the GABAA receptor-mediated response, presumably equal to the equilibrium potential of Cl−, were more depolarized than that in intact neurons. Thus, GABAA receptor-mediated excitation is suggested to be attributable to Cl− efflux out of the cell because of increased intracellular Cl− concentration ([Cl−]i) in axotomized neurons. Regulation of [Cl−]i in both control and injured neurons was disturbed by furosemide and bumetanide and by manipulating cation balance across the membrane, suggesting that functional alteration of furosemide-sensitive cation–Cl− cotransporters is responsible for the increase of [Cl−]i after axotomy.In situ hybridization revealed that neuron-specific K+-Cl− cotransporter (KCC2) mRNA was significantly reduced in the DMV after axotomy compared with that in control neurons. Similar expression of Na+, K+-Cl−cotransporter mRNA was observed between axotomized and control DMV neurons. Thus, axotomy led to disruption of [Cl−]i regulation attributable to a decrease of KCC2 expression, elevation of intracellular Cl−, and an excitatory response to GABA. A switch of GABA action from inhibitory to excitatory might be a mechanism contributing to excitotoxicity in injured neurons.

Reduction of KCC2 Expression and GABAAReceptor-Mediated Excitation after In Vivo Axonal Injury

Reduction of KCC2 Expression and GABA_AReceptor-Mediated Excitation after In Vivo Axonal Injury