The effects of electroconvulsive shock or imipramine on subtypes of α 1-adrenoceptors in the frontal cortex of the rat

Abstract

The effects of repeated treatment (14 days) with electroconvulsive shock (ECS) or imipramine on binding sites on α 1-adrenoceptors in the rat were studied. The binding of [ 3H]prazosin studied with WB4101 and phentolamine, as binding inhibitors, showed the existence of two subtypes of α 1-adrenoceptor (α 1A and α 1B). Proportions of the α 1A and α 1B binding sites were about 3:7 in the frontal cortex and 9:1 in the hippocampus. Pretreatment of the membranes with chlorethylclonidine (CEC) almost abolished the α 1B binding sites. Inhibition of the binding of [ 3H]prazosin studied with antidepressants (imipramine, desipramine, maprotiline and mianserin) showed that these drugs bound to α 1-adrenoceptors with low affinity, in an apparent monophasic manner. The characteristics of the α 1A and α 1B binding sites were studied by the binding assay with [ 3H]prazosin, in the presence of a small concentration (2 nM) of WB4101 to mask the α 1A binding sites, as well as the assay without WB4101, for the total α 1-adrenoceptor (α 1A and α 1B) binding. Repeated treatment with electroconvulsive shock increased but that with imipramine decreased, the density of the α 1B binding sites in the frontal cortex, without change of the affinity. Neither treatment affected the α 1A binding sites in the frontal cortex. The α 1adrenoceptors (α 1A and α 1B) in the hippocampus were not affected at all by these repeated treatments. The electroconvulsive shock-induced increase in the α 1B binding sites in the frontal cortex of the rat could contribute to differences in clinical effects between electroconvulsive shock and antidepressant drugs.