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Chronic cocaine treatment impairs the regulation of synaptosomal 3H-DA release by D2 autoreceptors.

作者信息

Yi S J, Johnson K M

机构信息

Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston 77550.

出版信息

Pharmacol Biochem Behav. 1990 Jul;36(3):457-61. doi: 10.1016/0091-3057(90)90241-9.

DOI:10.1016/0091-3057(90)90241-9
PMID:1974064
Abstract

The effect of repeated administration of cocaine on presynaptic D2 autoreceptor sensitivity in synaptosomes was studied. In rats treated chronically with saline, the dopamine D2 agonist 2-(N-propyl-N-2-thienylethylamino)-5-hydroxytetralin (N-0437) caused a significant inhibition of the Ca2(+)-evoked 3H-DA release from synaptosomes prepared from the nucleus accumbens and from the striatum; this effect was blocked by the D2 antagonist sulpiride. However, chronic cocaine pretreatment abolished the effect of N-0437 in both areas, suggesting a subsensitivity of release-modulating terminal DA autoreceptors. Subsensitive DA autoreceptors would enhance stimulated DA release from mesolimbic and nigrostriatal terminals and may play a role in the behavioral sensitization observed in this paradigm.

摘要

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