【摘 要】
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Objective TRPM7, as a divalent cation channel plays an important role in neurons damaged from cerebral ischemia due to permitting intracellular calcium overload.This study aimed to explore whether mag
【机 构】
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Department of Neurobiology and Key Laboratory of Neurological Disease of Hubei Province, Tongji Medi
【出 处】
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中国神经科学学会第九届全国学术会议暨第五届会员代表大会
论文部分内容阅读
Objective TRPM7, as a divalent cation channel plays an important role in neurons damaged from cerebral ischemia due to permitting intracellular calcium overload.This study aimed to explore whether magnesium was transported via TRPM7 channel into intracellular space of rat hippocampal neurons.Methods After 1 hour oxygen-glucose deprivation (OGD) and acute chemical ischemia (CI) by using methods of Mg2+ fluorescent probe Mag-Fura-2 to detect intracellular magnesium concentration ([Mg2+]i) and flame atomic absorption spectrometry to measure extracellular magnesium concentration ([Mg2+]o).Results The results showed that the neuronal [Mg2+]i was as 1.51 fold high after 1 h OGD as basal level and the increase of neuronal [Mg2+]i reached the peak after 1 h OGD and kept on for 60 min within re-oxygen.Meanwhile the [Mg2+]o decreased after 1 h OGD and recovered to the pre-ischemic level within 15 min after re-oxygen.In the situation of CI, the [Mg2+]i peak immediately appeared in hippocampal neurons.This increase of [Mg2+]i was declined by removing extracellular magnesium in OGD or CI.Furthermore, using Gd3+ or 2-APB to inhibit TRPM7 channels, [Mg2+]i increase which induced by OGD or CI was attenuated without altering basal level of [Mg2+]i.By silencing TRPM7 with shRNA in hippocampal neurons, it was found that not only the increase of [Mg2+]i induced by OGD or CI but also the basal level of [Mg2+]i were attenuated.In contrast, overexpression of TRPM7 in HEK293 cells exaggerated both the basal and increased [Mg2+]i after 1 h OGD/CI.Conclusion Results suggest that anoxia induce increase of [Mg2+]ivia TRPM7 channels in rat hippocampal neurons.
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