摘要

GABA, the main inhibitory neurotransmitter in the brain, elicits a hyperpolarizing response by activation of the GABA(A)-receptor/chloride-channel complex under conditions of normal Cl(-) homeostasis. Thus the pathogenesis of epilepsy could involve an impairment of GABA(A)-receptor-mediated inhibition due to a collapse of the Cl(-) gradient. We examined the expression patterns of Cl(-) transporters and a Cl(-) channel in a rat amygdala-kindling model. Activity-dependent increases were observed in the mRNA for NKCCl, an inwardly-directed Cl(-) transporter, in the piriform cortex. This suggests that an increase in [CL(-)](i) and a resultant reduction in GABAergic inhibition may occur in the kindled piriform cortex.

  • 出版日期2002-10