Taken in large doses, alcohol is considered to have anesthetic or depressive properties. It also has the ability to elicit euphoria when administered in small doses to susceptible persons (Be-gleiter and Porjesz, 1999). This phenomenon appears to be medi-ated by direct activation by alcohol of the mesolimbic dopamin-ergic circuit, particularly the ventral tegmental area (VTA) and the nucleus accumbens (NAc). Anxiolysis and relaxation also appear to be part of the spectrum of the rewarding effects of al-cohol, though these effects appear to be mediated by activation of the GABAergic neurotransmitter system.
In contrast to other addictive substances (e.g., nicotine, cocaine and opioids) and despite its significant effect on dopamin-ergic neurotransmission, the existence of specific alcohol binding sites on neuronal membranes has not been conclusively estab-lished. The lack of an alcohol receptor has led to the hypothesis that some alcohol effects, particularly those observed when it is administered at large doses, may be explained by disturbances in fluidity of the bi-layer lipid neuronal membrane. Changes in fluid-ity of neuronal membranesmayaffect the structure and functionof neurotransmitter receptors and ion channels. However, this hy-pothesis has failed to explain alcohol-rewarding effects that occur at lower doses.
On the other hand, alcohol administration appears to have effects across the major neurotransmitter systems (i.e., opioider-gic, serotonergic, GABAergic and glutamatergic). These systems are affected by both acute and chronic alcohol administration. They appear to play a major role in mediating the rewarding ef-fects of alcohol by modulating the firing of dopaminergic neu-rons in the VTA and the release of dopamine in the NAc.