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Influence of psychotomimetics and lisuride on synaptosomal dopamine release in the nucleus accumbens of rats.

European Journal of Pharmacology September 1, 1983 DOI: 10.1016/0014-2999(83)90140-1 (opens in new tab)

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AI-extracted from the abstract
Characteristics Peer reviewed
Population Crude synaptosomal fraction from the nucleus accumbens of rats
Interventions Lysergic acid diethylamide Mescaline N N-dimethyltryptamine Lisuride Haloperidol Methiothepine
Key points Lysergic acid diethylamide, mescaline, and N,N-dimethyltryptamine concentration-dependently inhibited potassium-evoked [3H]dopamine release from rat nucleus accumbens synaptosomes without affecting spontaneous release, while lisuride did not modulate release. Haloperidol or methiothepine antagonized the inhibition. The authors postulate the effect involves simultaneous action at presynaptic dopamine and 5-hydroxytryptamine receptors on dopamine nerve endings.

Abstract

In superfusion experiments with a crude synaptosomal fraction from the nucleus accumbens of rats, lysergic acid diethylamide, mescaline and N,N-dimethyltryptamine (representing different chemical classes of psychotomimetics) produced a concentration-related inhibition of K+-evoked [3H]dopamine release whereas spontaneous release remained unchanged. The nonpsychotomimetic ergoline lisuride tested at the same concentration range did not modulate spontaneous or K+-evoked [3H]dopamine release. The inhibitory effects of the psychotomimetics tested were antagonized by equal concentrations of haloperidol or methiothepine. It is postulated that the effects of psychotomimetics on DA release were triggered via simultaneous action at presynaptic dopamine and 5-hydroxytryptamine receptors which are located at dopamine nerve endings in the nucleus accumbens.

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