σ1 Receptors in rat striatum regulate NMDA-stimulated [3H]dopamine release via a presynaptic mechanism

Document Type

Journal Article

Publication Date

12-29-1995

Journal

European Journal of Pharmacology

Volume

294

Issue

2-3

DOI

10.1016/0014-2999(95)00617-6

Keywords

(+)-Pentazocine; BD1008 (N-[2-(3,4-dichlorophenyl)ethyl]-N-methyl-2-pyrrodinyl)cyclohexylamine); BD737 (1S,2R-(-)-N-[2-(3,4-dichlorophenyl)ethyl]-N-methyl-2-(1-pyrrolidinyl)cyclohexylamine); Dopamine release; DuP 734 (1-(cyclopropylmethyl)-4-(2′-(4″-fluorophenyl)-2′-oxoethyl)piperidine HBr); σ Receptor

Abstract

The role of the σ1 receptor in the regulation of N-methyl-d-aspartate (NMDA)-stimulated [3H]dopamine release from rat striatal slices was examined. The σ receptor agonist 1S,2R-(-)-N-[2-(3,4-dichlorophenyl)ethyl]-N-methyl-2-(1-pyrrolidinyl)cyclohexylamine (BD737) inhibited stimulated release in a concentration-dependent manner. The σ1 receptor antagonist, 1-(cyclopropylmethyl)-4-(2′-(4″-fluorophenyl)-2′-oxoethyl)piperidine HBr (DuP 734), reversed inhibition of release by BD737. Haloperidol, di-o-tolylguanidine (DTG) and N-[2-(3,4-dichlorophenyl)ethyl]-N-methyl-2-(1-pyrrolidinyl)ethylamine (BD1008) reversed the BD737-mediated inhibition of release. Haloperidol and DTG also antagonized inhibition of stimulated release by (+)-pentazocine. Furthermore, BD737 and (+)-pentazocine inhibited stimulated release in the presence of tetrodotoxin, suggesting that σ1 receptors regulating dopamine release are located on dopaminergic nerve terminals. These data suggest that σ1 receptors may be important in the regulation of glutamate-stimulated dopamine release. © 1995.

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