Kessler M, Terramani T, Lynch G, Baudry M
Center for the Neurobiology of Learning and Memory, University of California, Irvine 92717.
J Neurochem. 1989 Apr;52(4):1319-28. doi: 10.1111/j.1471-4159.1989.tb01881.x.
Membranes from rat telencephalon contain a single class of strychnine-insensitive glycine sites. That these sites are associated with N-methyl-D-aspartic acid (NMDA) receptors is indicated by the observations that [3H]glycine binding is selectively modulated by NMDA receptor ligands and, conversely, that several amino acids interacting with the glycine sites increase [3H]N-[1-(2-thienyl)cyclohexyl]piperidine ([3H]TCP) binding to the phencyclidine site of the NMDA receptor. The endogenous compound kynurenate and several related quinoline and quinoxaline derivatives inhibit glycine binding with affinities that are much higher than their affinities for glutamate binding sites. In contrast to glycine, kynurenate-type compounds inhibit [3H]TCP binding and thus are suggested to form a novel class of antagonists of the NMDA receptor acting through the glycine site. These results suggest the existence of a dual and opposite modulation of NMDA receptors by endogenous ligands.
大鼠端脑的膜含有一类对士的宁不敏感的甘氨酸位点。[3H]甘氨酸结合可被NMDA受体配体选择性调节,反之,几种与甘氨酸位点相互作用的氨基酸会增加[3H]N-[1-(2-噻吩基)环己基]哌啶([3H]TCP)与NMDA受体苯环己哌啶位点的结合,这些观察结果表明这些位点与N-甲基-D-天冬氨酸(NMDA)受体相关。内源性化合物犬尿氨酸以及几种相关的喹啉和喹喔啉衍生物抑制甘氨酸结合的亲和力远高于它们对谷氨酸结合位点的亲和力。与甘氨酸相反,犬尿氨酸类化合物抑制[3H]TCP结合,因此被认为是通过甘氨酸位点起作用的一类新型NMDA受体拮抗剂。这些结果表明内源性配体对NMDA受体存在双重且相反的调节作用。