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N-methyl-D-aspartate receptor-mediated contractions of the guinea pig ileum longitudinal muscle/myenteric plexus preparation: modulation by phencyclidine and glycine receptors

BG Campbell, P Couceyro, JF Keana and E Weber

Department of Physiology, Oregon Health Sciences University, Portland.

Glutamate evoked contractions of the longitudinal muscle/myenteric plexus (LMMP) preparation by an action at N-methyl-D-aspartate (NMDA) receptors. Other agonists at the NMDA recognition site, but not quisquilate or kainate, also contracted the LMMP, and glutamate-evoked contractions were competitively inhibited by selective NMDA receptor antagonists. Glutamate-evoked contractions were noncompetitively inhibited by MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo- [a,d]cyclohepten-5,10-imine moleate], phencyclidine (PCP) and other compounds that bind to the PCP receptor, which is a binding site on the NMDA channel complex. Their potencies for this effect were highly correlated with their affinities for the PCP receptor. Glycine significantly shifted the glutamate concentration-response curve to the left. Glycine site antagonists caused a glycine-sensitive, noncompetitive inhibition of glutamate-evoked contractions, and their potencies for this effect were highly correlated with their affinities for the glycine binding site of the NMDA channel complex. Mg++ and Zn++ also noncompetitively inhibited glutamate-evoked contractions. The modulatory effects of glycine, Mg++, Zn++ and PCP receptor ligands were specific to glutamate-evoked contractions. MK-801 was highly selective for inhibition of glutamate-evoked contractions; MK-801 also inhibited nicotinic responses at a 500-fold lower potency. Two novel compounds are described that bind to the PCP receptor with high affinity and selectively inhibit glutamate-evoked contractions in the LMMP.

Volume 257, Issue 2, pp. 754-766, 05/01/1991
Copyright © 1991 by American Society for Pharmacology and Experimental Therapeutics




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Copyright © 1991 by the American Society for Pharmacology and Experimental Therapeutics.