Smith S E, Gottfried J A, Chen J C, Chesler M
Department of Physiology and Biophysics, New York University Medical Center, NY 10016.
Neuroreport. 1994 Dec 20;5(18):2441-5. doi: 10.1097/00001756-199412000-00009.
Glutamate receptor activation induces an extracellular alkalinization in rodent hippocampus. We studied its Ca2+ dependence and pharmacology in hippocampal slices. Glutamate-evoked alkaline shifts were blocked by 0 Ca2+ saline. Alkalinizations induced by AMPA (alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) and NMDA (N-methyl-D-aspartate) were abolished by 20 microM CNQX (6-cyano-7-nitro-nitroquinoxaline-2,3-dione) and 50 microM APV (DL-2-amino-5-phosphonovalerate), respectively. The AMPA- and NMDA-evoked alkaline shifts were blocked by 0 Ca2+, however, AMPA-induced [K+]o elevation was unaffected. These data suggest that the glutamate receptor-channel does not mediate H+ influx, and support a role for Ca(2+)-H+ exchange.
谷氨酸受体激活可诱导啮齿动物海马体发生细胞外碱化。我们在海马体切片中研究了其对钙离子的依赖性及药理学特性。谷氨酸诱发的碱化转变可被无钙离子的生理盐水阻断。由α-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA）和N-甲基-D-天冬氨酸（NMDA）诱发的碱化分别被20微摩尔/升的6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX）和50微摩尔/升的DL-2-氨基-5-磷酸戊酸（APV）消除。AMPA和NMDA诱发的碱化转变可被无钙离子阻断，然而，AMPA诱导的细胞外钾离子浓度升高不受影响。这些数据表明谷氨酸受体通道不介导氢离子内流，并支持钙离子-氢离子交换的作用。
