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无镁诱导培养大鼠海马神经元癫痫放电模型中延迟整流钾电流的变化
  • 期刊名称:中国医科大学学报
  • 时间:2011.3.3
  • 页码:193-195
  • 分类:R96[医药卫生—药理学;医药卫生—药学]
  • 作者机构:[1]中国医科大学药学院药物毒理教研室,沈阳110001, [2]沈阳医学院生理教研室,沈阳110034
  • 相关基金:国家自然科学基金资助项目(81001429 31071004 30670761)
  • 相关项目:钙通道的钙调蛋白依赖性易化与失活的分子机制
中文摘要:

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。

英文摘要:

Objective To detect the changes in delayed rectifier K+ current in hippocampal neurons cultured in Mg2+-free medium in rat model of epileptiform discharge.Methods The hippocampal tissue was sampled from 1-day-old Wistar rats and used for the primary culture of hippocampla neurons.After 12 to 16 days of primary culture,the neurons were treated with Mg2+-free extracellular fluid for 3 hours,and then the discharge activity and delayed rectifier K+ current were recorded by patch clamp.Results After treated with Mg2+-free extracellular fluid,the neurons showed spontaneous "epileptiform discharge",and the delayed rectifier K+ current significantly increased.Conclusion The increase of delayed rectifier K+ current might be related to the underlying mechanism of spontaneous epileptiform discharge in hippocampal neurons cultured in Mg2+-free medium.

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