Figure 3.
Effects of alcohol and possible relevance to dependence and withdrawal. (A) The major acute actions of alcohol and their possible relation to the behavioral consequences of drinking alcohol are shown in relation to the Himmelsbach glutamate at N-methyl-d-aspartate (NMDA) receptors, and inhibition of voltage-operated calcium channels (VOCC’s) may underlie the relaxation, intoxication, anesthesia, and amnesia caused by alcohol. Alcohol also increases release of the neurotransmitter dopamine (DA) in a specific area of the brain, the nucleus accumbens. This action of alcohol is not very well understood but may play an important role in the rewarding effects of drinking, such as euphoria. (B) Examples of the adaptive changes thought to oppose the acute effects of alcohol. The bottom panels show possible consequences of these adaptations during withdrawal. For example, the adaptive changes in GABA receptor proteins caused by alcohol may make benzodiazepine tranquilizers, which also act on GABA receptors, less effective (i.e., may produce tolerance). A reduction in DA release in the nucleus accumbens may accompany alcohol withdrawal and may contribute to depression, anxiety, and emotional discomfort (i.e., dysphoria), perhaps leading an alcoholic to resume his or her drinking.
1CNS = central nevous system.