大鼠视网膜一氧化氮合酶神经元分布及缺血性损伤的改变

Nitric Oxide Synthase Neurons in the Rat Retina and Their Changes afterRetinal Ischemia

目的用还原型尼克酰胺腺嘌呤二核苷酸脱氢酶（ＮＡＤＰＨ）－黄递酶（ＮＤＰ）组化染色法研究大鼠视网膜一氧化氮合酶（ｎｉｔｒｉｃｏｘｉｄｅｓｙｎｔｈａｓｅ，ＮＯＳ）神经元的分布及缺血性损伤ＮＯＳ神经元的变化。方法动物模型采用升高眼内压的方法造成视网膜缺血。摘除眼球后，剥离视网膜，进行ＮＡＤＰＨ－ＮＤＰ反应。结果正常大鼠视网膜ＮＯＳ阳性神经元仅分布于内核层内侧，呈散在分布，具有较长的串株样突起。视网膜缺血１０、３０、６０ｍｉｎ组ＮＯＳ阳性神经元同对照组相比形态学改变及计数均无显著性差异（Ｐ＞０．０５）；而缺血９０ｍｉｎ组，ＮＯＳ阳性神经元数量减少，与对照组相比有显著性差异（Ｐ＜０．０５）。结论正常大鼠视网膜ＮＯＳ阳性神经元散在分布于内核层内侧，可能是无长突细胞；视网膜缺血早期ＮＯＳ阳性神经元无明显变化，提示一氧化氮（ＮＯ）可能不介导ＮＭＤＡ受体激活所致的细胞毒性，缺血晚期数量减少则可能由于ＮＯＳ阳性神经元死亡。

ObjectiveTo investigate nitric oxide synthase(NOS) neurons in the rat retina and its changes after different periods of retinal ischemia using NADPHNDP histochemistry.MethodsThe retinal ischemia was produced by elevated intraocular pressure which was about 110 mm Hg.The rats were divided into 5 groups,i.e.ischemia for 10,30,60,90 min and normal control.NADPHNDP staining was performed on flat preparations of retinas.ResultsNOS positive neurons were distributed in the inner nuclear layer (INL) with long beadlike processes.No significant difference was found in groups of 10,30,60 min after retinal ischemia comparing to the normal retinas.In group of 90 min after retinal ischemia,NOS neurons decreased remarkably (P<0.05).ConclusionNOS positive neurons were in the INL of normal rat retina,and possibly were amacrine cells.No remarkable changes were found after a short period of retinal ischemia,which indicates nitric oxide(NO) might not mediate NMDA receptor activated cytotoxicity.The late cell loss is probably due to ischemiainduced NOS neuronal cell death.