Altered response to cessation of nerve impulse flow in dopamine neurons after chronic ethanol administration.

Rats were chronically treated with ethanol for 150 and 270 days, respectively. The influence of chronic ethanol treatment on the activation of tyrosine hydroxylation (measured as the accumulation of dopa after inhibition of amino acid decarboxylase) produced by gamma-butyrolactone (GBL) was studied. It appeared that the ability of GBL to enhance the dopa accumulation was attenuated in rats subjected to ethanol, thus indicating that subsensitivity will develop at or beyong GABA receptors following chronic ethanol treatment. Preliminary findings concerning the effects of chronic ethanol administration on dopamine autoreceptor sensitivity are also reported.