Static, transient and permanent organization of GABAA receptor expression in calbindin‐positive interneurons in response to amygdala kindled seizures

We tested the hypothesis that experimentally produced epilepsy (by kindling) may induce changes in GABAA receptor expression in some but not all interneuron populations. Using laser capture microdissection and quantitative polymerase chain reaction (QPCR) analysis, GABAA receptor α subunit expression in calbindin‐ (CBir) and parvalbumin‐ (Parvir) 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, Cbir neurons in the hilus and/or perirhinal cortex up‐regulated the expression of α2, α3 and α5 subunit mRNAs up to 900%. In contrast, no changes were found in Parvir neurons. In Cbir neurons contralateral to the amygdala kindling site α1 subunit mRNA expression was increased. In both Cbir and Parvir 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 α2 protein was up‐regulated in the processes but not in the cell somas of calbindin‐positive neurons, whereas α3 subunit protein expression was up‐regulated on the cell bodies of Cbir neurons in the hilus. These data indicate that different interneuron populations may selectively reorganize their GABAA subunit expression in response to seizures.