Abolition of the NMDA-mediated responses by a specific glycine antagonist, 6,7-dichloroquinoxaline-2,3-dione (DCQX).
Among various quinoxaline derivatives examined, only 6,7-dichloroquinoxaline-2,3-dione (DCQX) competitively displaced the strychnine-insensitive binding of [3H]glycine, without affecting the other binding sites on the N-methyl-D-aspartate (NMDA) receptor complex. This novel specific antagonist abolished the ability of L-glutamate to potentiate [3H]MK-801 binding activity in brain synaptic membranes treated with Triton X-100. Inclusion of glycine reversed this preventive action of DCQX on the potentiation induced by glutamate.
Yoneda
Y
Y
Department of Pharmacology, Setsunan University, Osaka, Japan.
Ogita
K
K
D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism / Q000494:pharmacology; D001665:Binding Sites; D001667:Binding, Competitive; D001921:Brain / Q000378:metabolism; D005998:Glycine / Q000037:antagonists & inhibitors*; D007700:Kinetics; D016202:N-Methylaspartate; D011810:Quinoxalines / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter / Q000187:drug effects / Q000378:metabolism*; D013329:Structure-Activity Relationship; D013570:Synaptic Membranes / Q000187:drug effects / Q000378:metabolism*
D011810:Quinoxalines; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D001224:Aspartic Acid; D016202:N-Methylaspartate; C061603:6,7-dichloroquinoxaline-2,3-dione; D005998:Glycine