Marvizón J C, Lewin A H, Skolnick P
Laboratory of Neuroscience, NIDDK, Bethesda, MD 20892.
J Neurochem. 1989 Mar;52(3):992-4. doi: 10.1111/j.1471-4159.1989.tb02554.x.
1-Aminocyclopropane carboxylic acid (ACPC) competitively inhibited (IC50, 38 +/- 7 nM) [3H]glycine binding to rat forebrain membranes but did not affect [3H]strychnine binding to rat brainstem/spinal cord membranes. Like glycine, ACPC enhanced 3H-labelled (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate ([3H]MK-801) binding to N-methyl-D-aspartate receptor-coupled cation channels (EC50, 135 +/- 76 nM and 206 +/- 78 nM for ACPC and glycine, respectively) but was approximately 40% less efficacious in this regard. The maximum increase in [3H]MK-801 binding produced by a combination of ACPC and glycine was not different from that elicited by glycine, but both compounds potentiated glutamate-stimulated [3H]MK-801 binding. These findings indicate that ACPC is a potent and selective ligand at the glycine modulatory site associated with the N-methyl-D-aspartate receptor complex.
1-氨基环丙烷羧酸（ACPC）竞争性抑制（IC50，38±7 nM）[3H]甘氨酸与大鼠前脑细胞膜的结合，但不影响[3H]士的宁与大鼠脑干/脊髓膜的结合。与甘氨酸一样，ACPC增强了3H标记的（+）-5-甲基-10,11-二氢-5H-二苯并[a,d]环庚烯-5,10-亚胺马来酸盐（[3H]MK-801）与N-甲基-D-天冬氨酸受体偶联阳离子通道的结合（ACPC和甘氨酸的EC50分别为135±76 nM和206±78 nM），但在这方面的效力约低40%。ACPC和甘氨酸联合产生的[3H]MK-801结合的最大增加与甘氨酸引起的无差异，但两种化合物均增强了谷氨酸刺激的[3H]MK-801结合。这些发现表明，ACPC是与N-甲基-D-天冬氨酸受体复合物相关的甘氨酸调节位点上的一种强效和选择性配体。
