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目的:通过神经损伤性噪声引起4周昆明小鼠出现暂时性阈移(TTS)和永久性阈移(PTS),探讨听觉通路N-甲基D-天冬氨酸受体(NMDAR)活性调节耳蜗螺旋神经节(CG)磷酸化c-Jun变化。方法:采用30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,并采用免疫组织化学对耳蜗听觉通路中NMDAR关键成分(磷酸化c-Jun)的表达进行检测。结果:噪声性聋诱导PTS后8h、48h、7d、14dCG磷酸化c-Jun的相对吸收度值明显增加,而阳性细胞数依次减少。噪声性聋诱导PTS前后立即腹膜腔注射MK-801引起相似改变。而诱导TTS后48h则降至正常水平。结论:磷酸化c-Jun在噪声性聋后表达的增加具有时间相关性;MK-801通过阻断噪声暴露后传入神经递质谷氨酸,减少突触后钙内流所致的兴奋性毒性,从而保护听觉神经。因此,NMDAR可能参与了内耳损伤。
OBJECTIVE: To investigate the transient threshold shift (TTS) and permanent threshold shift (PTS) in Kunming mice induced by nerve injury noise and to investigate the regulation of N-methyl D-aspartate receptor (NMDAR) activity in auditory pathway Cochlear spiral ganglion (CG) phosphorylation of c-Jun changes. Methods: Thirty Kunming mice were used to make animal models of noise-induced deafness. Auditory brainstem response was detected by immunohistochemistry. The expression of key components of NMDAR (phosphorylated c-Jun) in cochlear auditory pathway was detected by immunohistochemistry. Results: The relative absorbance of phosphorylated c-Jun of CG at 8h, 48h, 7d and 14d after noise-induced deafness was significantly increased, while the number of positive cells decreased. A similar change was induced by peritoneal injection of MK-801 immediately before and after induction of deafness. 48h after induction of TTS was reduced to normal levels. CONCLUSION: The time-dependent expression of phosphorylated c-Jun increases after noise-induced deafness. MK-801 can block the release of glutamate and reduce the excitability induced by the postsynaptic calcium influx Toxicity, thereby protecting the auditory nerve. Therefore, NMDAR may be involved in inner ear damage.