Sun D Y, Li X P
Department of ENT, Third Hospital, Beijing Medical University, Beijing 100083.
Lin Chuang Er Bi Yan Hou Ke Za Zhi. 2000 Aug;14(8):373-4.
To study the effect of NO in noise-induced deafness.
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.
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.
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.
研究一氧化氮在噪声性聋中的作用。
采用NADPH - 黄递酶组织化学染色、NOSmRNA原位杂交及Northern印迹分析观察噪声暴露对豚鼠耳蜗中NOSmRNA表达的影响。
NADPH - 黄递酶组织化学显示，NOS主要存在于豚鼠耳蜗的内毛细胞、柯蒂氏器的外毛细胞、螺旋神经节细胞及血管纹边缘细胞中；NOSmRNA原位杂交表明，在内毛细胞、外毛细胞及螺旋神经节细胞中有阳性信号，但在血管纹边缘细胞中无阳性信号；Northern印迹显示，噪声暴露组的表达比对照组更强。
耳蜗传入通路中可能存在谷氨酸：NMDA受体、一氧化氮：环磷酸鸟苷途径；噪声暴露诱导一氧化氮过量产生介导神经毒性作用；血管纹边缘细胞产生并释放一氧化氮以调节耳蜗的微循环。
