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汉防己碱对缺血神经元钾通道的作用 |
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王中峰*薛春生**
摘 要 目的和方法：研究汉防己碱(Tet)对缺血状态下大鼠皮层神经元膜电压依赖性钾通道变化的影响。方法：分离大鼠皮层神经元和建立细胞贴附膜片钳技术。结果：在缺血状态下，钾通道开放时间常数τ1和τ2分别由对照组的0.429 ms和8.209 ms增加至1.855 ms和17.464 ms(P＜0.01)，开放概率由0.114增加到0.151(P＜0.01)。Tet(7.5，15和30 μmol/L)浓度依赖性抑制由缺血所诱导的钾通道开放。Tet 7.5和15 μmol/L改变了通道的关闭模式，30 μmol/L改变了通道的开放模式。结论：缺血可导致神经元电压依赖性钾通道开放显著增加，对胞外钾离子聚积起重要作用，从而参与神经元的损伤，Tet可抑制上述改变而对缺血脑细胞产生保护作用。
主题词 局部缺血；神经元；钾通道
The effects of tetrandrine on neuronal potassium channel in ischemia-like condition
WANG Zhong-Fong, XUE Chun-Sheng
Department of Physiology, Third Military Medical University,Chongqing (400038)
Abstract AIM: To study the effects of tetrandrine(Tet) on changes of rat cortical neuronal potassium channel in ischemia-like condition. METHODS:Acutely isolated rat cortical neurons and single channel recording of patch clamp technique. RESULTS:Compared with control group, the open time constants τ1 and τ2 of potassium channels of rat cortical neurons increased from 0.429 ms and 8.209 ms to 1.855 ms and 17.464 ms, respectively (P all ＜0.01). Open-state probability increased from 0.114 to 0.151（P＜0.01).Tet (7.5, 15 and 30 μmol/L) significantly inhibited the open of potassium channel induced by ischemia-like condition in concentration-dependent maner. Tet in 30 μmol/L changed the open model,15 and 7.5 μmol/L changed the close model. CONCLUSION:The prolonged open of potassium channels in ischemia-like condition would result in extracellular K+ assembling, which play an important role in cerebral injury. Tet protected the cerebral injury by inhibiting the long-lasting open of potassium channel induced by ischemia-like condition.
MeSH Ischemia; Neurons; Potassium channels
脑缺血时，细胞内外离子的分布平衡失调，在细胞内钙聚积的同时，发现胞外K+堆积，从而使胞内外钾离子的浓度梯度减小，细胞膜的静息电位降低，导致细胞兴奋性提高，细胞过度去极化，参与了脑缺血细胞损伤［1，2］。钾通道的亚型很多，对它们在缺血时胞外钾聚集的作用研究较少。有实验证实汉防己碱(tetrandrine, Tet)对缺血脑有保护作用［3］，本文用缺氧缺糖来模拟缺血，用膜片钳技术研究Tet对缺血状态下大鼠大脑皮层神经[1] [2] 下一页
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