Amygdala kindling induces upregulation of mRNA for NKCC1, a Na+, K+–2Cl− cotransporter, in the rat piriform cortex

GABA, the main inhibitory neurotransmitter in the brain, elicits a hyperpolarizing response by activation of the GABAA-receptor/chloride-channel complex under conditions of normal Cl− homeostasis. Thus the pathogenesis of epilepsy could involve an impairment of GABAA-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 NKCC1, 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. [Copyright &y& Elsevier]