Indexed on: 01 May '88Published on: 01 May '88Published in: Neurochemical Research
Ethanol (10–200 mM) transiently increased tritium overflow from superfused rat nucleus accumbens slices previously incubated with [3H]dopamine (DA) and [14C]choline. The effect was greater in striatal tissue and did not appear to be a non-specific membrane effect since [14C]acetylcholine (ACh) release was not affected. Lack of antagonism by picrotoxin suggested that γ-aminobutyric acid (GABA) receptors were not involved. Calcium was not a requirement and the DA uptake blocker, nomifensine, was without effect. Ethanol appeared to be causing [3H]DA release into the cytoplasm. K+-stimulated release of [3H]DA and [14C]ACh from nucleus accumbens and striatal slices was not affected. Clonidine-mediated inhibition of the K+-evoked release of [3H]DA remained unaltered. Ethanol attenuated the isoproterenol-induced enhancement of [3H]DA release. Ethanol therefore appeared to interact with components of the DA terminal causing a transient increase in the release of neurotransmitter without impairing K+-evoked release but apparently interfering with the isoproterenol-induced effect.