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Ethanol and the GABAA Receptor-Gated Chloride Ion Channel

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Neuropharmacology of Ethanol

Abstract

The cellular (viz., biochemical and neurophysiological) mechanisms underlying the behavioral (e.g., intoxicating, anxiolytic and sedative/hypnotic) actions of ethanol are not well understood. Ethanol has many of the physiochemical properties of other anesthetic agents, conferring non-specific disordering effects on neuronal membranes, especially at high concentrations. It is generally acknowledged that ethanol shares more specific pharmacologic actions with other sedative/hypnotic drugs such as the barbiturates and benzodiazepines. These include anxiolytic, anticonvulsant and sedative activity (Liljequist and Engel, 1984) and in certain behavioral paradigms, the development of cross tolerance and cross dependence (Boisse and Okamoto, 1980; Le et al., 1986). These findings suggest that ethanol, barbiturates and benzodiazepines may share at least one common mechanism of action.

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© 1991 Springer Science+Business Media New York

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Morrow, A.L., Montpied, P., Paul, S.M. (1991). Ethanol and the GABAA Receptor-Gated Chloride Ion Channel. In: Meyer, R.E., Lewis, M.J., Koob, G.F., Paul, S.M. (eds) Neuropharmacology of Ethanol. Birkhäuser, Boston, MA. https://doi.org/10.1007/978-1-4757-1305-3_3

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  • DOI: https://doi.org/10.1007/978-1-4757-1305-3_3

  • Publisher Name: Birkhäuser, Boston, MA

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