Chronic ethanol treatment uncouples striatal calcium entry and endogenous dopamine release.
Chronic ethanol treatment resulted in a marked reduction in the release of dopamine from striatal synaptosomes in response to depolarization. Calcium entry into the same synaptosomal preparations was not altered. Calculation of the ratio of calcium entry vs dopamine release showed that, under control conditions, approximately 15 calcium ions were required to cause the release of 1 dopamine molecule. Chronic ethanol treatment increased this ratio to more than 80:1, suggesting that chronic ethanol administration altered the coupling between calcium entry and dopamine release. Addition of ethanol in vitro to synaptosomes isolated from chronic ethanol-treated rats returned this ratio to approximately 20:1. These results suggest that chronic ethanol treatment results in dependence which is reflected biochemically in striatum through changes in the coupling between voltage-dependent calcium entry into nerve endings and subsequent neurotransmitter release.
D000437:Alcoholism / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D003342:Corpus Striatum / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism*; D008297:Male; D008564:Membrane Potentials; D051381:Rats; D013574:Synaptosomes / Q000378:metabolism
D002118:Calcium; D004298:Dopamine