ELECTROCONVULSIVE SHOCK INCREASES ALPHA-1B-ADRENOCEPTOR BY NOT ALPHA-1A-ADRENOCEPTOR BINDING-SITES IN RAT CEREBRAL-CORTEX

Repeated administration of electroconvulsive shock (ECS) increases [H-3]prazosin binding to alpha-1-adrenoceptors in rat cerebral cortex. In contrast, [H-3]WB4101 binding in cortex has been reported to be unchanged after ECS. [H-3]Prazosin labels two alpha-1-adrenoceptor subtypes, termed alpha-1a and alpha-1b, whereas [H-3]WB4101 labels the alpha-1a subtype preferentially. The purpose of this study was to determine whether ECS increases one or both alpha-1-adrenoceptor subtypes in rat cerebral cortex. We found that treatment of rats with ECS once daily for 10-12 days increased [H-3]prazosin binding in cortex by about 25% but did not significantly alter [H-3]WB4101 binding to alpha-1a-adrenoceptors. Measurement of alpha-1a and alpha-1b receptors by competition analysis of the selective alpha-1a antagonist 5-methlurapidil against [H-3]prazosin and measurement of [H-3]prazosin binding in homogenates preincubated with chlorethylclonidine, which alkylates alpha-1b binding sites, also indicated that the ECS-induced increase in alpha-1-adrenoceptors is confined to the alpha-1b subtype. In contrast to its effect on [H-3]prazosin binding, ECS did not increase phosphoinositide hydrolysis as measured by [H-3]inositol 1-phosphate accumulation in slices of rat cerebral cortex stimulated by either norepinephrine or phenylephrine. The failure of ECS to increase [H-3]inositol 1-phosphate accumulation stimulated by phenylephrine, which is a partial agonist for this response, suggests that spare receptors do not account for the apparent absence of effect of ECS on alpha-1-adrenoceptor-mediated phosphoinositide hydrolysis.