Ogita K, Yoneda Y
Department of Pharmacology, Setsunan University, Osaka, Japan.
Biochem Biophys Res Commun. 1988 Jun 16;153(2):510-7. doi: 10.1016/s0006-291x(88)81124-0.
Pretreatment of brain synaptic membrane homogenates with Triton X-100 resulted in a drastic disclosure of [3H] glutamate (Glu) binding activity which was sensitive to one of the central Glu receptor agonists, N-methyl-D-aspartic acid (NMDA). The NMDA-sensitive binding was inversely dependent on the incubation temperature, and was a reversible and saturable process. Scatchard analysis revealed that Triton X-100 treatment yielded in a significant enhancement of the affinity with a concomitant increment of the density of binding sites. Electrophysiologically identified agonists and antagonists for the NMDA receptors all significantly inhibited the binding to Triton-treated membranes. These results suggest that Triton-treatment may disclose NMDA-sensitive [3H] Glu binding sites in brain synaptic membranes.
用Triton X-100预处理脑突触膜匀浆，导致[3H]谷氨酸（Glu）结合活性显著暴露，该活性对中枢Glu受体激动剂之一N-甲基-D-天冬氨酸（NMDA）敏感。NMDA敏感结合与孵育温度呈负相关，是一个可逆且可饱和的过程。Scatchard分析表明，Triton X-100处理使亲和力显著增强，同时结合位点密度增加。电生理学鉴定的NMDA受体激动剂和拮抗剂均显著抑制与Triton处理膜的结合。这些结果表明，Triton处理可能揭示脑突触膜中NMDA敏感的[3H] Glu结合位点。
