Abstract
For several years, the major hypothesis to explain the behavioral effects of ethanol has been the “membrane hypothesis” (HUNT 1985).This postulate is based on work demonstrating that ethanol, which is an amphipathic substance, can penetrate into and perturb the structure of (“fluidize”) cell membrane lipids (CHIN and GOLDSTEIN 1977; HARRIS and SCHROEDER 1981). While there is evidence to suggest that bulk lipid perturbation may be involved in the high-dose, hypnotic, or anesthetic effects of ethanol (GOLDSTEIN et al. 1982), this nonspecific interaction of ethanol with biological systems does not well explain low-dose effects of ethanol such as intoxication, ataxia, or reinforcement. Recent research has demonstrated that the function of certain neurochemical systems, notably those which consist of multiple membrane-associated protein subunits (e.g., the GABAA receptor, receptor-coupled adenylate cyclase), is very sensitive to modulation by low concentrations of ethanol. These systems have been designated “receptive elements” for ethanol (TABAKOFF and HOFFMAN 1987). Knowledge that the function of particular neurochemical systems is sensitive to modification by ethanol allows investigators to develop hypotheses regarding the neurochemical basis for certain behavioral responses to low doses of ethanol, based on the involvement of the neurochemical systems in the particular behavior (e.g., ethanol potentiation of GABAA receptor-coupled ion flux might be expected to contribute to the anxiolytic effect of ethanol).
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Hoffman, P.L. (1995). Effects of Alcohol on Excitatory Amino Acid Receptor Function. In: Kranzler, H.R. (eds) The Pharmacology of Alcohol Abuse. Handbook of Experimental Pharmacology, vol 114. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-78435-4_4
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