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目的：研究“缺血”大鼠大脑大皮层神经元Ｎ－甲基－Ｄ－天冬氨酸（ＮＭＤＡ）受体通道的单通道变化特征。方法：细胞贴附式膜片钳技术。结果：在“缺血”状态下，ＮＭＤＡ受体通道３５ｐＳ和１００ｐＳ电导水平的开放概率分别由对照组的０．０７９±０．００６和０．０６７±０．００４增加到０．３０８±０．１５５和０．４８８±０．１２６（Ｐ＜０．０１），３５ｐＳ通道开放时间常数τ２由对照值（４．１７±０．３８）ｍｓ增加到（８．５４±２．０５）ｍｓ（Ｐ＜０．０１），关闭时间由（７５．５０±１４．１０）ｍｓ缩短到（１１．８０±４．３０）ｍｓ（Ｐ＜０．０１）。结论：“缺血”可显著开放大鼠大脑皮层神经元ＮＭＤＡ受体通道，使钙内流增加，对胞内钙超载起重要作用，此可能是脑缺血细胞损伤的机制之一。
Aim: To study the single-channel changes of N-methyl-D-aspartate (NMDA) receptor channel in the cerebral cortex of ischemic rats. Methods: Cell attachment patch clamp technique. Results: The open probability of 35pS and 100pS conductance of NMDA receptor channel increased from 0.079 ± 0.006 and 0.067 ± 0.004 in control group to 0.308 ± 0 in “ischemic” state. 155 and 0.488 ± 0.126 respectively (P <0.01). The open time constant τ2 of 35pS channel increased from 4.17 ± 0.38 ms to 8.54 ± 2.05 ms (P <0.01), and the closing time decreased from (75.50 ± 14.10) ms to (11.80 ± 4.30) ms (P <0.01). CONCLUSION: “Ischemia” can significantly open the NMDA receptor pathway in rat cerebral cortex neurons, increase the influx of calcium and play an important role in intracellular calcium overload, which may be one of the mechanisms of cerebral ischemia injury.