DEVELOPMENT OF FUNCTIONAL DEPENDENCE ON ETHANOL IN DOPAMINERGIC SYSTEMS

  • 1 January 1979
    • journal article
    • research article
    • Vol. 208  (2) , 216-222
Abstract
Withdrawal of mice from chronic ethanol treatment results in a decreased responsiveness of striatal (but not mesolimbic) dopamine-sensitive adenylate cyclase activity to stimulation by dopamine. This subsensitivity is not apparent at the time of withdrawal from chronic feeding of ethanol, when animals are still intoxicated, but becomes evident as ethanol is eliminated from the animals. Addition of ethanol in vitro to tissue homogenates from ethanol-withdrawn animals, at concentrations similar to those found in the brain at the time of withdrawal, normalizes the response of the adenylate cyclase to dopamine. No difference is evident between control and ethanol-withdrawn animals in stimulation of adenylate cyclase by sodium fluoride. The specificity of the response of striatal adenylate cyclase to stimulation by dopamine, as compared to other transmitters, is unaltered by chronic ethanol feeding. Chronic treatment with ethanol and withdrawal also does not affect the specific binding of spiroperidol in either striatal or mesolimbic regions. The decreased response of adenylate cyclase to dopamine in ethanol-withdrawn animals may result from decreased efficiency of coupling between dopamine receptor sites and catalytic units of adenylate cyclase.