Nishizaki T, Matsuoka T, Nomura T, Kondoh T, Tamaki N, Okada Y
Department of Physiology, Department of Neurosurgery, Kobe University School of Medicine, 7-5-1 kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.
Biochem Biophys Res Commun. 1999 Jun 16;259(3):661-4. doi: 10.1006/bbrc.1999.0520.
NMDA produced whole-cell membrane currents in cultured human astrocytes. The currents were not inhibited by the selective NMDA receptor antagonist, APV, while they were partially inhibited by the broad G-protein inhibitor, GDPbetaS. NMDA-induced currents were enhanced by either the microsomal Ca2+/ATPase inhibitors, thapsigargin and cyclopiazonic acid, or the ATP-uncoupler, dinitrophenol (DNP). In the Ca2+ assay, NMDA increased intracellular calcium concentration. The increase was inhibited by 26% in Ca2+-free extracellular solution, and it was not inhibited by APV. The results of the present study suggest that NMDA responses in human astrocytes are regulated by store Ca2+ depletion-associated signal.
N-甲基-D-天冬氨酸（NMDA）在培养的人星形胶质细胞中产生全细胞膜电流。这些电流不受选择性NMDA受体拮抗剂APV的抑制，而被广泛的G蛋白抑制剂GDPβS部分抑制。NMDA诱导的电流可被微粒体Ca2+/ATP酶抑制剂毒胡萝卜素和环匹阿尼酸或ATP解偶联剂二硝基苯酚（DNP）增强。在Ca2+检测中，NMDA增加细胞内钙浓度。在无Ca2+的细胞外溶液中，这种增加被抑制了26%，并且它不受APV的抑制。本研究结果表明，人星形胶质细胞中的NMDA反应受储存Ca2+耗竭相关信号的调节。
