摘要
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 +
Aim: To make approach to the relationship between the changes of free zinc and ischemic neuronal damage in hippocampus after forebrain ischemia/reperfusion. Methods: The models of forebrain ischemia/reperfusion were established in rats. The contents of free Zn 2+ were measured by TSQ fluorescence method. The Zn 2+ chelator (CaEDTA) was injected into lateral ventricles in order to evaluate the effect of free Zn 2+ on ischemic neuronal damage.Results: ①Zn 2+ fluorescence in the hilus of dentate gyrus, CA3 region and the stratum radiatum and stratum oriens of CA1 decreased slightly at forty eight hours after reperfusion. From seventy two hours to ninety six hour after reperfusion, the decreased fluorescence gradually returned to the normal level, but some fluorescence dots were found in pyramidal neurons of CA1 and the hilus of dentate gyrus. Seven days after reperfusion, all the changes of the fluorescence almost recovered. ②The cell membrane impermeable Zn 2+ chelator CaEDTA could reduce the intracellular concentration of free Zn 2+ and reduced neuronal damage after forebrain ischemia/reperfusion. Conclusion: ①The synaptic vesicle Zn 2+ released and then translocated into postsynaptic neurons after forebrain ischemia/reperfusion and played a role in ischemic neuronal damage. ②The cell membrane impermeable chelator CaEDTA could provide neuroprotection.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2002年第3期222-225,共4页
Chinese Journal of Applied Physiology
