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目的 :探讨前脑缺血 /再灌注后海马结构游离Zn2 + 变化与神经元缺血性迟发损伤之间的关系。方法 :建立大鼠前脑缺血 /再灌注模型 ;采用TSQ荧光法检测海马神经元内游离Zn2 + 变化 ;观察侧脑室注入Zn2 + 螯合剂对海马结构神经元内游离Zn2 + 含量和对其病理变化的影响。结果 :①再灌注后 4 8h ,CA3区、齿状回门、CA1区起层和放射层的Zn2 + 荧光强度较缺血前减弱 ;再灌注后 72～ 96h海马结构背景荧光强度恢复至缺血前水平 ,但在CA1区和齿状回门锥体细胞层出现逐渐增多的斑点状荧光 ;再灌注后 7d ,荧光强度基本恢复正常 ;②侧脑室内注入Zn2 + 螯合剂CaEDTA能降低细胞内游离Zn2 + 含量 ,减轻海马CA1区神经元损伤。结论 :①前脑缺血 /再灌注后 ,海马神经元突触前末梢游离Zn2 + 的释放和扩散增加 ,Zn2 + 移位至突触后神经元并参与神经元缺血性损伤 ;②膜不通透性Zn2 + 螯合剂CaEDTA可减轻海马神经元缺血性损伤
Objective: To investigate the relationship between changes of free Zn2 + in hippocampal formation and ischemic delayed neuronal injury after forebrain ischemia / reperfusion in rats. Methods: The model of forebrain ischemia / reperfusion in rats was established. The changes of free Zn2 + in hippocampal neurons were detected by TSQ fluorescence spectrophotometry. The contents of free Zn2 + in hippocampal neurons and the expression of Zn2 + The impact of change. RESULTS: At 48 h after reperfusion, the fluorescence intensity of Zn2 + in the CA3 zone, dentate gyrus, CA1 zone and radioactive layer was weaker than that before ischemia, and the fluorescence intensity of hippocampal formation returned to ischemia at 72-96 h after reperfusion But there was a gradually increasing speckled fluorescence in the CA1 area and the dentate gyrus cell layer. Fluorescence intensity returned to normal after 7 days of reperfusion; ② Intraventricular injection of Ca2 + + chelator CaEDTA reduced intracellular free Zn2 + content, reduce neuronal damage in CA1 area of hippocampus. Conclusions: ①The release and proliferation of free Zn2 + in the presynaptic terminals of hippocampal neurons increases after forebrain ischemia / reperfusion, and Zn2 + translocates to postsynaptic neurons and participates in neuronal ischemic injury. Permeable Zn2 + chelator CaEDTA can reduce ischemic injury of hippocampal neurons