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Selectivity of Ethanol's Actions on Brain Receptor Systems: Catecholamines and Ethanol
Author(s) -
Tabakoff B.,
Hoffman P.L.,
Valverius P.,
Nhamburo P.T.,
Saito T.
Publication year - 1988
Publication title -
australian drug and alcohol review
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.018
H-Index - 74
eISSN - 1465-3362
pISSN - 0819-5331
DOI - 10.1080/09595238880000101
Subject(s) - chemistry , ethanol , receptor , physical dependence , adenylate kinase , agonist , g protein , adrenergic receptor , pharmacology , biochemistry , biophysics , medicine , biology , morphine
A parsimonious hypothesis of ethanol's actions in the brain focuses attention on the general ability of amphipathic molecules to perturb neuronal membrane lipid order. An analysis of the effects of ethanol and other anesthetics on beta‐adrenergic receptor coupled adenylate cyclase (AC) activity in brain membranes, however, indicates a selectivity of ethanol's actions on receptor‐effector coupling proteins such as the guanine nucleotide (GN) binding proteins N s and N i and demonstrates differences in the effects of alcohols on AC activity as compared to actions of other anesthetic agents (chloroform and halothane). The acute effects of ethanol on certain information‐transducing systems of brain may thus be mediated by rather specific interactions with microdomains or “receptive” areas of neuronal membranes. The chronic effects of ethanol on the beta‐adrenergic receptor coupled AC in mouse cortex were characterized by changes in beta‐agonist binding kinetics and by the decreased ability of isoproterenol to stimulate AC activity. The changes induced by chronic ethanol ingestion were reminiscent of heterologous desensitization of the beta‐adrenergic receptor. Thus, both acute and chronic ethanol administration may produce changes in adrenergic function in brain which may, in turn, be associated with ethanol intoxication or the development of tolerance or dependence