Alteration in expression of G-protein-activated inward rectifier K+-channel subunits GIRK1 and GIRK2 in the rat brain following electroconvulsive shock

G-protein-activated inward rectifier potassium channels are coupled to a nu mber of neurotransmitter receptors, including some monoamine receptors. In the present study we have investigated the effect of electroconvulsive shoc k on gene expression of the G-protein-activated inward rectifier potassium channel subunits G-protein-coupled inward rectifier K+-channel (GIRK1) and GIRK2 in the rat brain using in situ hybridization and immunocytochemistry. Acute electroconvulsive shock (a single shock) increased GIRK2 expression while causing a transient reduction of the messenger RNA abundance of GIRK1 in granule cells of the dentate gyrus. Chronic electroconvulsive shock (fi ve shocks over 10 days) caused a larger increase in GIRK2 messenger RNA abu ndance, which was accompanied by an increase in GIRK2 immunoreactivity in t he molecular layer of the dentate gyrus. Unlike for acute electroconvulsive shock, GIRK1 messenger RNA abundance in the dentate gyrus was significantl y increased after chronic electroconvulsive shock. No significant alteratio ns in GIRK1 and GIRK2 messenger RNA abundance were detected in the other br ain regions studied, including the CA1 and CA3 subfields of the hippocampus , the frontal-parietal cortex and piriform cortex. The neuroanatomically specific changes in expression of the potassium chann el subunits may directly influence neuronal excitability as well as the fun ctions of G-protein-coupled neurotransmitter receptors. (C) 1999 IBRO. Publ ished by Elsevier Science Ltd.