全脑缺血早期大鼠海马各区域小白蛋白免疫反应阳性中间神经元的不同时相变化的定量分析

QUANTITATIVE ANALYSIS OF TIME DEPENDENT CHANGES OF PARVALBUMINIMMUNOREACTIVE INTERNEURONS IN DIFFERENT SECTORS OF RAT HIPPOCAMPUS EARLY AFTER CEREBRAL ISCHEMIA

近十几年来，缺血性脑损伤的细胞分子机制已成为神经科学界的重要研究内容之一。本实验用免疫组织化学定量分析方法对四管阻塞造成的全脑缺血20min后再灌流0～24h的大鼠海马小白蛋白中间神经元的变化进行了观察。结果显示：再灌流0～6h之间CA2、CA3区小白蛋白阳性中间神经元均出现一过性减少．到24h时恢复三缺血前水平：而CA1区小白蛋白阳性中间神经元的减少出现于再灌流12h后。此外齿状回颗粒层及门区小白蛋白阳性中间神经元变化不显著。本实验结果提示，短暂性全脑缺血早期海马各区域小白蛋白阳性神经元减少的不同时相特征．可能与海马各区域的不同缺血敏感性及不同缺血的病理学表现有关。

Neuroscientists have focused their attention on the molecular and cellular mechanism of cerebral ischemia for morethan ten years. We investigated postischemic changes of parvalbumin immunoreactive (PV-ir) interneurons in the rat hippocampus 0 h-24 h after 20 min of 4 vessel obstruction cerebral ischemia, with PV immunohistochernistry. Transient reductions ofPV-ir interneurons were seen both in the hippocampal CA2 and CA3 sectors between 0 h～6 h after ischemia. They rapidly returned to preischemic levels 24 h after ischemia. A marked loss of PV-ir interneurons was seen in the hippocampal CA1 sector 12h after ischemia. Furthermore. a slightly but no significantly decrease of staining occurred in the dentate granular layer andhilus. Our results demonstrate that the different time dependent PV-ir interneuron reduction seen in different sectors of hippocampus early after cerebral ischemia may be Telated to the different vulnerability to ischemia and different pathologic changesafter ischemia.