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目的利用无镁细胞外液诱导原代培养大鼠海马神经元癫痫放电模型来检测延迟整流钾电流的变化。方法采用新生24 h内Wistar大鼠,分离海马神经元进行原代培养。体外培养至12~16 d时,无镁细胞外液处理神经元3 h并恢复正常细胞外液,应用全细胞膜片钳技术记录神经元的放电情况及延迟整流钾电流。结果无镁处理后的神经元存在自发的“癫痫样”放电;无镁诱导可使神经元延迟整流钾电流增大。结论延迟整流钾电流增大可能与无镁诱导体外培养大鼠海马神经元自发异常放电的基础病理机制相关。
OBJECTIVE: To detect the change of delayed rectifier potassium current by inducing primary epileptic rat hippocampal neuronal discharge model by using magnesium-free extracellular fluid. Methods Primary cultured Wistar rats were isolated from hippocampal neurons of neonatal rats for 24 h. After cultured in vitro for 12-16 days, the neurons were treated with magnesium-free extracellular fluid for 3 h and the normal extracellular fluid was recovered. The whole-cell patch clamp technique was used to record the neuronal discharge and delayed rectifier potassium current. Results Magnesium-free neurons had spontaneous “epileptiform” discharges. Magnesium-induced neurotransmission delayed rectifier potassium currents. Conclusion The increase of delayed rectifier potassium current may be related to the basic pathological mechanism of spontaneous abnormal discharge of hippocampal neurons induced by magnesium in vitro.