We tested the hypothesis that experimentally produced epilepsy (by kindling) may induce changes in GABA(A) receptor expression in some but not all interneuron populations. Using laser capture microdissection and quantitative polymerase chain reaction (QPCR) analysis, GABA(A) receptor alpha subunit expression in calbindin- (CBir) and parvalbumin- (Parv(ir)) immunoreactive interneurons was compared between normal brains and brains in which amygdala kindled seizure responses were permanently established. Two weeks after the last seizure response, Cb-ir neurons in the hilus and/or perirhinal cortex up-regulated the expression of alpha(2), alpha(3) and alpha(5) subunit mRNAs up to 900%. In contrast, no changes were found in Parv(ir) neurons. In Cb-ir neurons contralateral to the amygdala kindling site alpha1 subunit mRNA expression was increased. In both Cb-ir and Parv(ir) neurons, the coordinated subunit expression patterns ipsilateral (fully kindled) and contralateral (partially kindled) to the kindling site suggested that permanent and transient co-expressional relationships occur respectively. In the perirhinal cortex alpha2 protein was up-regulated in the processes but not in the cell somas of calbindin-positive neurons, whereas alpha3 subunit protein expression was up-regulated on the cell bodies of Cb-ir neurons in the hilus. These data indicate that different interneuron populations may selectively reorganize their GABA(A) subunit expression in response to seizures.