Neurotransmitter function in the basal ganglia after acute and chronic ethanol treatment

Abstract

Acute and chronic administration of ethanol has multiple effects on several neurotransmitters in the basal ganglia. Dopamine is the transmitter predominantly affected. Acceleration of dopaminergic activity is observed at low doses of ethanol. However, at high doses the reverse is observed. During the ethanol withdrawal syndrome that develops after chronic treatment, dopaminergic responses are reduced, whether from presynaptic or postsynaptic origins. Evidence also indicates that cholinergic and GABAergic processes may be implicated in these actions of ethanol. Ethanol apparently induces a variety of alterations in neurotransmitter function as a result of its disruption of membrane structure and associated electric properties.