Hippocampal and Cerebellar β‐Adrenergic Receptors and Adenylate Cyclase Are Differentially Altered by Chronic Ethanol Ingestion

Abstract

Chronic ethanol ingestion by mice resulted in the loss of high-affinity .beta.-adrenergic agonist binding sites and a significant decrease in activation of adenylate cyclase by guanine nucleotides and .beta.-adrenergic agonists in the hippocampus, although no significant change was noted in the total number of .beta.-adrenergic receptors, as defined by the binding of the antagonist [125I]iodocyanopindolol. In cerebellum, chronic ethanol ingestion resulted in a 16% decrease in the total concentration of .beta.-adrenergic receptors and in a decrease in the affinity for agonist of the high-affinity .beta.-adrenergic agonist binding sites. However, neither the amount of the high-affinity agonist binding sites nor the activation of adenylate cyclase by agonist was affected. The different responses to ethanol in hippocampus and cerebellum may result from quantitative differences in distribution of .beta.1- and .beta.2-adrenergic receptors in the tested brain areas and/or differential effects of ethanol on stimulatory guanine nucleotide binding protein in these brain areas.