Glutamic Acid Synaptic Activity is a Target of Acute and Chronic Ethanol Effects in the Mammalian Brain

Abstract

Acute ethanol intake is known to affect a multiplicity of physiological processes that control neuronal excitability in both the central and peripheral nervous systems. It is quite obvious that the actions of ethanol on central and peripheral neurons cannot be explained by a single molecular mechanism, nor should they be attributed to a single physiological change. Neuronal excitability is a very dynamic process that is dependent on many metabolic activities to provide the milieu in which the sudden alteration of the biophysical states of macromolecules may produce changes in membrane ion conductance, transmitter release, or receptor activation. These dynamic events are disrupted when ethanol, present in either the external or internal environment of the cell, alters either the metabolic state of a neuron or the physicochemical properties of macromolecules that have an important function in nerve cell excitability. It is well known that ethanol has rather wide-spread effects on cell metabolism (13) and that it interacts with a variety of macromolecules or macro-molecular arrays, including proteins and lipids found in intracellular and plasma cell membrances (20).