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Vol. 53, Issue 4, 684-690, April 1998
Shanghai Institute of Cell Biology, 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 
-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 ~7-fold, from 6 to 40 nM), and the maximal response induced by DPDPE was reduced
by ~60%. The effects of NMDA were reversible, and the DPDPE response
could recover within 60 min. The functional responses of -, µ-,
and 
-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 stimulated Gi
2 phosphorylation. Transient
transfection into NG108-15 cells of the wild-type Gi2 and a mutated Gi2 (Ser144Ala) resulted in a 2-fold
increase in DPDPE-stimulated G protein activation. The DPDPE responses were greatly inhibited by NMDA treatment in the wild-type
Gi2-transfected cells but much less affected in the
mutant Gi2-transfected cells. In summary, NMDA
attenuates opioid receptor/G protein coupling, and this process
requires activation of PKC.
Copyright © 1998 by The American Society for Pharmacology and Experimental Therapeutics
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