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目的通过噪声引起4周龄昆明小鼠出现暂时性阈移(tmporary threshold shift,TTS)和永久性阈移(permanent threshold shift,PTS),观察听觉通路耳蜗螺旋神经节神经元(spiral ganglion of cochlea,CG)中生长相关蛋白(growth associated protein 43,GAP-43)变化,探讨听觉损伤后内耳突触修复的可能机制。方法采用32只昆明小鼠制作噪声性聋动物模型,进行听觉脑干诱发反应听力检测,用免疫组化法对耳蜗听觉通路中GAP-43在神经损伤刺激的表达进行检测。结果噪声性聋引起PTS后CG的GAP-43表达在损伤后第7天出现增加,第14天仍增加明显,而TTS组无明显变化。结论噪声性聋听觉通路神经性损伤作用后7天,GAP-43出现增高说明内耳开始出现突触修复。
Objective To observe the effects of noise on the transient threshold shift (TTS) and permanent threshold shift (PTS) of Kunming mice at 4 weeks of age. To observe the effect of auditory pathway on cochlear spiral ganglion neurons (spiral ganglion of cochlea, CG), and to explore the possible mechanism of synaptic repair after auditory injury. Methods 32 Kunming mice were used to make animal model of noise-induced deafness. The auditory brainstem response was detected by immunohistochemistry. The expression of GAP-43 in nerve stimulation of cochlear auditory pathway was detected by immunohistochemistry. Results The expression of GAP-43 in CG induced by noise-induced deafness increased on the 7th day after injury, but still significantly increased on the 14th day, but no significant change in the TTS group. Conclusion The increased appearance of GAP-43 on the 7th day after the noise-induced deafness of auditory pathway can explain the initiation of synaptic repair in the inner ear.