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目的:通过建立实验性变态反应性神经炎这一周围神经脱髓鞘动物模型,观察其听神经病变,初步探讨其听性脑干反应(ABR)和听神经复合动作电位(CAP)的改变。方法:以粗提的牛外周神经髓鞘碱性蛋白(MBP)作为抗原,免疫实验组豚鼠;对照组以生理盐水代替MBP。检测动物血清抗MBPIgG水平、坐骨神经传导速度,观察坐骨神经、听神经病理改变;检测ABR、CAP阈值及潜伏期;观察内耳病理损伤。结果:实验组血清抗MBPIgG水平升高,与对照组相比P<0.01;实验组坐骨神经传导速度减慢,与对照组相比P<0.05;透射电镜发现坐骨神经、听神经脱髓鞘改变;免疫前后实验组14只(26耳)出现ABR反应阈升高,伴Ⅰ、Ⅲ、Ⅴ波潜伏期明显延长,与对照组比较P<0.01,而Ⅰ～Ⅲ、Ⅲ～Ⅴ波间期与对照组比较P>0.05;CAPN1、N1波潜伏期延长,与对照组比较P<0.01;另有4只(8耳)仅出现潜伏期延长而无阈值升高;免疫组织化学显示内耳免疫损伤部位主要在蜗神经、内耳神经纤维、螺旋神经节;扫描电镜显示内毛细胞纤毛紊乱、胞质溢出。结论:实验性变态反应性神经炎动物模型作为一种可靠的周围神经脱髓鞘动物模型,其病变可累及听神经出现听神经脱髓鞘改变,ABR和CAP阈值升高、潜伏期明显延长,该模型可望成为探讨听神经脱髓鞘的听力学表现的一种有用的动物模型。
OBJECTIVE: To establish an animal model of peripheral nerve demyelination with experimental allergic neuritis and observe its auditory neuropathies and to investigate the changes of auditory brainstem response (ABR) and auditory nerve complex action potential (CAP). Methods: Crude bovine peripheral nerve myelin basic protein (MBP) was used as an antigen to immunize the guinea pigs in experimental group. The control group was given physiological saline instead of MBP. The serum levels of anti-MBPIgG, sciatic nerve conduction velocity, sciatic nerve and auditory nerve pathology were detected. The ABR and CAP threshold and latency were measured. The pathological changes of the inner ear were observed. Results: The level of anti-MBPIgG in the experimental group was significantly higher than that in the control group (P <0.01). The conduction velocity of the sciatic nerve in the experimental group was slower than that of the control group (P <0.05), and the sciatic nerve and auditory nerve demyelination were found by transmission electron microscopy In the experimental group, the ABR threshold increased with the increase of the ABR response threshold. The latencies of Ⅰ, Ⅲ and Ⅴ waves were significantly prolonged compared with the control group (P <0.01), while the phases of Ⅰ ~ Ⅲ and Ⅲ ~ > 0.05. The latency of CAPN1 and N1 wave prolonged, compared with the control group (P <0.01). In addition, the latency of CAPN1 and N1 increased only with no increase of threshold value. Immunohistochemistry revealed that the inner ear immunostaining was mainly located in the cochlear nerve, Nerve fibers, spiral ganglia; scanning electron microscopy showed ciliated hair cells disorders, cytoplasm overflow. Conclusion: The animal model of experimental allergic neuritis, as a reliable animal model of peripheral nerve demyelination, can affect the auditory nerve demyelination in the lesion. The threshold of ABR and CAP is increased and the incubation period is prolonged. It is a useful animal model to investigate the audiological manifestation of auditory nerve demyelination.