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Vol. 304, Issue 1, 364-369, January 2003

sigma 1 Receptor Agonist-Mediated Regulation of N-Methyl-D-aspartate-Stimulated [3H]Dopamine Release Is Dependent upon Protein Kinase C

Samer J. Nuwayhid and Linda L. Werling

Department of Pharmacology, The George Washington University Medical Center, Washington, DC

We have previously shown that sigma 1 receptor agonists inhibit N-methyl-D-aspartate (NMDA)-stimulated [3H]dopamine from slices of rat striatum in a concentration-related manner and that the inhibition is reversed by sigma 1 receptor-selective and nonsubtype-selective sigma  receptor antagonists. Based on previous evidence from our laboratory as well as other laboratories, we hypothesized that sigma 1 receptors might use a protein kinase C (PKC) signaling pathway to modulate stimulated dopamine release. We tested several inhibitors of PKC isozymes, as well as a phospholipase C inhibitor for their effects on sigma 1 receptor agonist-mediated regulation of [3H]dopamine release. Although none of the inhibitors tested affected the ability of NMDA to stimulate [3H]dopamine release, they all abolished regulation by the sigma 1 receptor agonist (+)-pentazocine in a concentration-related manner. We also found that prior exposure to 1 µM phorbol 2-myristate 13-acetate for 30 min abolished regulation by (+)-pentazocine. We concluded that an intact PKC system was required for sigma 1 agonist-mediated regulation of NMDA-stimulated [3H]dopamine release from rat striatal slices. Based on the pharmacological profile of the PKC inhibitors tested, as well as reports in the literature on PKC involvement in neurotransmitter release and sigma  receptor action, PKCbeta seems most likely to be responsible, at least in part, for the effects of (+)-pentazocine on dopamine release.

0022-3565/03/3041-0364$07.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 2003 by The American Society for Pharmacology and Experimental Therapeutics


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