摘要
目的 :探讨一氧化氮 ( NO)在噪声性聋发病中的作用。方法 :用中高频连续稳态噪声制作噪声性聋的动物模型 ,用 NADPH-黄递酶组织化学、原位杂交和 Northern印迹法 ,观察噪声刺激对耳蜗一氧化氮合酶 ( NOS)表达的影响。结果 :组织化学法显示 NOS主要分布于内外毛细胞、螺旋神经节细胞和血管纹边缘细胞 ;原位杂交法发现 NOSm RNA在内外毛细胞、螺旋神经节细胞胞浆内均可见阳性染色 ,但血管纹边缘细胞无阳性染色 ;Northern印迹法显示实验组 NOSm RNA表达较对照组增强。结论 :听觉传入径路上存在 Glu:NMDA受体 ,NO:c GMP通路 ,噪声刺激诱发的 NO合成具有介导神经中毒作用 ,血管纹边缘细胞能合成一定量 NO。
Objective:To study the effect of NO in noise-induced deafness. Method:The effect of noise exposure on the expression of NOSmRNA in the guinea pig cochlea was observed with NADPH diaphorase histochemistry staining,NOSmRNA hybridization in situ and Northern blotting analysis.Result:NADPH diaphorase histochemistry indicated that NOS mainly presents in the inner hair cells, outer hair cells of Corti′s organ, spiral ganglion cells and the marginal cells of stria vascularis in the guinea pig cochlea; NOSmRNA hybridization in situ showed that there is positive signal in the inner hair cells, outer hair cells and spiral ganglion cells, but there is no positive signal in the stria marginal cells of vascularis; Northern blotting showed that the expression of noise exposure group is more intensive than that of the control group.Conclusion:There is a Glu :NMDA receptor ,NO: cGMP pathway in the cochlear afferent possibly; noise exposure induced overproduction of NO mediates the effect of neurotoxicity; the marginal cells of stria vascular produce and release NO to regulate the microcirculation of the cochlea.
出处
《临床耳鼻咽喉科杂志》
CSCD
2000年第8期373-374,共2页
Journal of Clinical Otorhinolaryngology
关键词
一氧化氮
一氧化氮合酶
耳蜗
噪声
Nitric oxide Nitric oxide synthase Cochlea Noise