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Related Experiment Videos

Receptor-mediated dopaminergic function after ethanol withdrawal.

R F Black, P L Hoffman, B Tabakoff

    Alcoholism, Clinical and Experimental Research
    |July 1, 1980
    PubMed
    Summary
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    Chronic ethanol exposure and withdrawal impair dopamine (DA) synthesis and release regulation in mice. This suggests ethanol disrupts the signaling pathway between dopamine receptors and the enzyme tyrosine hydroxylase.

    Area of Science:

    • Neuroscience
    • Pharmacology
    • Neurochemistry

    Background:

    • Striatal dopamine (DA) synthesis is regulated by interactions with dopamine receptors.
    • Neuroleptics and DA agonists modulate DA synthesis via these receptors.
    • Ethanol's effects on this regulatory system are not fully understood.

    Purpose of the Study:

    • To investigate the impact of chronic ethanol treatment and withdrawal on DA synthesis and release regulation.
    • To assess the functional state of dopamine receptors and their coupling to DA synthesis machinery.

    Main Methods:

    • Developed a sensitive high-performance liquid chromatography (HPLC) technique for in vivo measurement of DOPA accumulation (as a marker of DA synthesis) and DA levels.
    • Administered DA antagonist haloperidol and DA agonist apomorphine to C57BL mice after chronic ethanol exposure and withdrawal.

    Related Experiment Videos

  • Evaluated changes in DOPA accumulation and DA release in response to these pharmacological challenges.

    • Main Results:

    • Chronic ethanol treatment and withdrawal significantly decreased DOPA accumulation in response to both haloperidol and apomorphine.
    • Ethanol exposure also reduced DA release induced by these agents.
    • The observed alterations in response were not consistent with DA receptor subsensitivity or supersensitivity.

    Conclusions:

    • Ethanol treatment and withdrawal perturb the coupling between dopamine receptors and tyrosine hydroxylase, a key enzyme in DA synthesis.
    • This disruption in receptor-ligand-enzyme signaling may underlie altered dopaminergic function observed after chronic ethanol exposure.