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Ethanol-induced narcosis was studied in mice as a function of pretreatment with L-dopa and its metabolites administered alone or in conjunction with Ro-4-4602, an inhibitor of aromatic- L-amino acid decarboxylase. These studies suggest that L-dopa prolongation of ETOH narcosis in mice may be due to formation of one or more toxic metabolites rather than to a direct involvement of dopamine. Ethanol narcosis also was studied in mice as a function of age of animals, concentration of ETOH, ambient temperature and saline pretreatment. Since manipulation of these variables produced alterations in ETOH narcosis, the need for their rigid control is indicated.

Clinical Pharmacology & Therapeutics (1996) 59, 183–183; doi:

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