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本文以体外分散培养的新生大鼠海马ＣＡ１区神经细胞为标本，分别采用激光扫描共聚焦显微镜动态监测单个细胞［Ｃａ２＋］ｉ和膜片箝全细胞记录的电生理技术检测细胞的ＮＭＤＡ电流和电压依赖性Ｃａ２＋电流等方法，较为深入地研究了抑制性神经递质γ－氨基丁酸（ＧＡＢＡ）及ＧＡＢＡ－Ａ受体激动剂蝇蕈醇（Ｍｕｓｃｉｍｏｌ）对急性缺氧时海马ＣＡ１神经元［Ｃａ２＋］ｉ升高过程的影响方式及其作用机制。结果表明：对照组细胞缺氧后比缺氧前［Ｃａ２＋］ｉ升高２６８％±６８％（ｎ＝５）；而以２０μｍｏｌ／ＬＧＡＢＡ或２０μｍｏｌ／ＬＭｕｓｃｉｍｏｌ作用的细胞在缺氧后［Ｃａ２＋］ｉ升高仅分别为２６％±９％（ｎ＝５）和４０％±１５％（ｎ＝５），与对照组相比均有极显著差异（Ｐ＜０．００１）。说明它们具有抑制缺氧引起的神经元［Ｃａ２＋］ｉ升高的作用。在膜片箝的全细胞记录实验中，观察到２０μｍｏｌ／ＬＧＡＢＡ能够抑制ＮＭＤＡ电流，对其幅度的抑制率为６３．３±１１．６％（ｎ＝５）；别外，２０μｍｏｌ／ＬＧＡＢＡ对由－９０－０ｍＶ脉冲电压诱发的Ｃａ２＋电流最大峰值的抑制率为５４．８％±１０．７％（ｎ＝５）。以往的实验证据揭示，ＮＭＤＡ受体耦联的离子通道和电?
In this study, the neurons of hippocampal CA1 area of neonatal rats were cultured in vitro. The dynamic changes of NMDA current and voltage were measured by laser scanning confocal microscopy and the whole cell recording of single cells [Ca2 +] i and patch clamp. Dependent Ca2 + currents, the effect of inhibitory neurotransmitter γ-aminobutyric acid (GABA) and GABA-A receptor agonist Muscimol on hippocampal CA1 neurons [Ca2 + ] I increase the impact of the process and its mechanism of action. The results showed that the cells in control group were 268% ± 68% (n = 5) higher than those in [Ca2 +] i before hypoxia, whereas those in cells treated with 20μmol / L GABA or 20μmol / (N = 5) and 40% ± 15% (n = 5), respectively. There were significant differences (P <0.001) compared with the control group. Indicating that they have a hypoxia-induced increase in the role of [Ca2 +] i neurons. In patch-clamp whole-cell recording experiments, it was observed that 20μmol / LGABA could inhibit the NMDA current with an amplitude of 63.3 ± 11.6% (n = 5). In addition, 20μmol / The maximal inhibitory rate of Ca2 + induced by -90-0mV pulse voltage was 54.8% ± 10.7% (n = 5). Previous experimental evidence revealed that NMDA receptor-coupled ion channels and electron?