Hood W F, Compton R P, Monahan J B
Central Nervous System Diseases Research, G.D. Searle & Co., St. Louis, MO 63198.
Neurosci Lett. 1989 Mar 13;98(1):91-5. doi: 10.1016/0304-3940(89)90379-0.
We have previously shown that D-cycloserine displaces [3H]glycine binding to a recognition site with properties consistent with an N-methyl-D-aspartate (NMDA) receptor modulatory site. Additionally, D-cycloserine positively modulates the NMDA receptor as evidenced by its dose-dependent enhancement of [3H]1-[1-(2-thienyl)cyclohexyl]piperidine ([3H]TCP) binding to the NMDA receptor-coupled ionophore. Further evaluation of this compound indicates that the maximal stimulation of [3H]TCP binding induced by D-cycloserine is lower than that produced by other compounds acting at the NMDA receptor associated glycine modulatory site (glycine and D-serine). Moreover, the stimulation of [3H]TCP binding induced by D-cycloserine in the presence of various fixed concentrations of glycine results in a family of dose-response curves which asymptotically converge to 40-50% of the maximal stimulation induced by glycine alone. These results are consistent with D-cycloserine acting as a partial agonist of the NMDA receptor via its interaction with the coupled glycine modulatory site.
我们之前已经表明,D-环丝氨酸能取代[3H]甘氨酸与一个识别位点的结合,该位点的特性与N-甲基-D-天冬氨酸(NMDA)受体调节位点一致。此外,D-环丝氨酸能正向调节NMDA受体,这一点可通过其对[3H]1-[1-(2-噻吩基)环己基]哌啶([3H]TCP)与NMDA受体偶联离子通道结合的剂量依赖性增强得到证明。对该化合物的进一步评估表明,D-环丝氨酸诱导的[3H]TCP结合的最大刺激低于作用于NMDA受体相关甘氨酸调节位点的其他化合物(甘氨酸和D-丝氨酸)所产生的刺激。此外,在各种固定浓度的甘氨酸存在下,D-环丝氨酸诱导的[3H]TCP结合刺激产生了一系列剂量反应曲线,这些曲线渐近地收敛到单独甘氨酸诱导的最大刺激的40-50%。这些结果与D-环丝氨酸通过与偶联的甘氨酸调节位点相互作用而作为NMDA受体的部分激动剂的作用一致。