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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Protective effect of GV150526A on the glutamate-induced changes in basal and electrically-stimulated cytosolic Ca++ in primary cultured cerebral cortical cells.
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Protective effect of GV150526A on the glutamate-induced changes in basal and electrically-stimulated cytosolic Ca++ in primary cultured cerebral cortical cells.

机译：GV150526A对谷氨酸诱导的原代培养的大脑皮层细胞基础和电刺激的胞质Ca ++变化的保护作用。

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摘要

Glutamate-induced changes in intracellular free Ca++ concentration ([Ca++]i) were recorded in resting and electrically-stimulated primary cultures of rat cerebral cortical cells, employing the Ca++ indicator Fura 2. A brief (10 min) exposure to glutamate led to a concentration-dependent basal [Ca++]i increase, measured 30 min after glutamate removal. In order to unmask more subtle modifications in [Ca++]i movements associated with neurosecretion, the glutamate effect was also studied in electrically-stimulated cells. The application of trains (10 s) of electrical pulses (intensity 30 mA, duration 1 ms) induced frequency-related Na+- and Ca++-dependent [Ca++]i transients. A 5 min treatment with 50 microM glutamate reduced to 48% the electrically-evoked [Ca++]i transients, evaluated 30 min after glutamate challenge. The neuroprotective effect of sodium 4,6-dichloro-3-[(E)-3-(N-phenyl)propenamide]indole-2-carboxylate (GV150526A), a new indole derivative with high affinity and selectivity for the glycine site of the NMDA receptor-channel complex, was compared with that of DL-2-amino-5-phosphonopentanoic acid (AP5), ifenprodil, 7-chlorokynurenic acid and 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)-quinoxaline (NBQX) on glutamate-induced [Ca++]i changes in resting and electrically-stimulated cells. In both experimental conditions, GV150526A showed to be the most potent compound. Moreover, GV150526A and 7-chlorokynurenic acid were 2-3 times more active in stimulated neurons than in resting neurons, indicating a major involvement of the glycine site in the protection of the cells kept in an active state.
机译：谷氨酸诱导的细胞内游离Ca ++浓度（[Ca ++] i）的变化记录在大鼠的大脑皮层细胞的静息和电刺激的原始培养物中，采用Ca ++指示剂Fura2。短暂（10分钟）暴露于谷氨酸导致了谷氨酸去除后30分钟测得的浓度依赖性基础[Ca ++] i增加。为了揭示与神经分泌有关的[Ca ++] i运动的更微妙的修饰，在电刺激的细胞中也研究了谷氨酸的作用。电脉冲序列（10 s）（强度30 mA，持续时间1 ms）的应用引起了与频率相关的Na +和Ca ++依赖性[Ca ++] i瞬变。用谷氨酸激发后30分钟评估，用50μM谷氨酸的5分钟处理将电诱发的[Ca ++] i瞬变降低至48％。 4,6-二氯-3-[（E）-3-（N-苯基）丙烯酰胺]吲哚-2-羧酸钠（GV150526A）的神经保护作用，这是一种新型吲哚衍生物，对甘氨酸的甘氨酸位点具有高亲和力和选择性。将NMDA受体通道复合物与DL-2-氨基-5-膦基戊酸（AP5），艾芬地尔，7-氯尿嘧啶酸和2,3-二羟基-6-硝基-7-氨磺酰基苯并（f）-喹喔啉（NBQX）对谷氨酸诱导的[Ca ++] i的改变在静息和电刺激的细胞中。在两种实验条件下，GV150526A均显示是最有效的化合物。此外，GV150526A和7-氯尿嘧啶酸在受刺激的神经元中的活性是静止神经元的2-3倍，这表明甘氨酸位点在保护处于活动状态的细胞中起主要作用。

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