PMID: 9547359May 9, 1998Paper

N-Methyl-D-aspartate attenuates opioid receptor-mediated G protein activation and this process involves protein kinase C

Molecular Pharmacology
G H FanG Pei

Abstract

The effects of N-methyl-D-aspartate (NMDA) on opioid receptor-mediated G protein activation were explored in neuroblastoma X glioma hybrid (NG108-15) cells. Treatment of the cells with NMDA resulted in a remarkable attenuation of [35S]guanosine-5'-O-(3-thio)triphosphate binding stimulated by [D-Pen2,D-Pen5]-enkephalin (DPDPE), a delta-opioid receptor agonist. The effects of NMDA were dose and time dependent with an IC50 value of 5 nM and could be blocked by NMDA receptor antagonists. After NMDA treatment, the DPDPE dose-response curve shifted to the right (EC50 value increased approximately 7-fold, from 6 to 40 nM), and the maximal response induced by DPDPE was reduced by approximately 60%. The effects of NMDA were reversible, and the DPDPE response could recover within 60 min. The functional responses of delta-, mu-, and kappa-opioid receptors in primarily cultured neurons also were attenuated significantly by NMDA treatment. The inhibitory effects of NMDA on opioid receptor-mediated G protein activation could be blocked by coadministration of the protein kinase C (PKC) inhibitors or by elimination of the extracellular Ca2+. Correspondingly, NMDA treatment of NG108 cells significantly elevated cellular PKC activity and stimula...Continue Reading

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Citations

Sep 20, 2017·Clinical and Experimental Pharmacology & Physiology·Shahrdad Lotfipour, Maree T Smith
Jul 8, 1999·Proceedings of the National Academy of Sciences of the United States of America·K LingG Pei
Jun 7, 2006·The International Journal of Neuroscience·Mohammad-Reza ZarrindastAmeneh Rezayof
Jun 3, 2000·Annual Review of Pharmacology and Toxicology·P Y LawH H Loh
Jul 12, 2002·British Journal of Pharmacology·Reza N SharifMarian E Fundytus

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