Electroconvulsive shock and reserpine: effects on beta-adrenergic receptors in rat brain.

Abstract

Electroconvulsive shock (ECS) administered once daily for up to 14 days decreases beta-adrenergic receptor binding in the cortex and hippocampus in a time-dependent manner. The decrease in binding in the cortex lasts at least 1 week after the last shock. In the striatum, hypothalamus, or cerebellum, 14 days of ECS did not produce significant changes in beta-adrenergic receptor binding. The brain regional pattern of beta-adrenergic receptor changes suggests that repeated ECS affects beta 1-adrenergic receptors in brain regions that receive a noradrenergic innervation activated by ECS. The effects of ECS on neurotransmitter receptor binding appear to be highly selective. Of five receptors in the cortex and three receptors in the hippocampus measured, only beta-adrenergic receptor binding is decreased. Chronic footshock stress does not alter beta-adrenergic receptor binding sites in the cortex, indicating that the effects of ECS are not due to stress alone. The effects of ECS on reserpine-induced alterations in beta-adrenergic receptor binding sites were also examined. Ten days of ECS following chronic reserpine injections reverses the increased binding of beta-adrenergic receptors.