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目的通过前庭代偿的动物模型,了解在前庭病变的情况下,前庭传出性和传入性神经系统的相互作用。方法动物模型A组(16只)为正常大鼠。B组(15只)左侧前庭损毁术后7d。C组(7只)术后3个月。D组(7只)前庭代偿后。检测两侧头长肌静息状态的肌电图。检测传出性前庭神经系统降钙素基因相关肽免疫组化。检测传出性前庭神经系统胆硷乙酰转移酶(cholineacetyltransferase,AChT)免疫组化。检测传入性前庭神经系统NaKATP酶活性。结果损伤同侧肌群肌电活动减弱、对侧肌群增强,前庭代偿期恢复对称性。急性期传出性前庭神经系统降钙素基因相关肽阳性细胞双侧性增多,活性增高。传出性前庭神经系统损伤同侧AChT阳性反应细胞减少,两侧反应程度增加。前庭代偿期对侧反应程度显著增加。急性期同侧NaKATP酶mRNA表达水平低,对侧前庭信号增强,在前庭代偿期,同侧NaKATP酶mRNA表达水平增强,与对侧一致或略强。结论传出性前庭神经系统可能抑制对侧前庭传入信息,调整同侧前庭中枢兴奋性,在前庭代偿的复杂机制中发挥作用。
Objectives To understand the interaction of vestibular efferent and afferent nervous systems in the context of vestibular disorders through an animal model of vestibular compensation. Methods Animal model group A (16 rats) were normal rats. Group B (15) left vestibular injury after 7d. Group C (7) after 3 months. Group D (7) after vestibular compensation. Electromyography to detect the rest of the head long muscles on both sides. Detection of calcitonin gene-related peptide immunohistochemistry in the outgoing vestibular system. The expression of AChT was detected by immunohistochemistry in the outgoing vestibular nervous system. Detection of afferent vestibular nervous system NaKATP enzyme activity. Results The injured ipsilateral muscle group myoelectric activity decreased, the contralateral muscle group enhanced vestibular compensatory phase recovery symmetry. Acute phase of the vestibular calcitonin gene-related peptide positive cells increased bilateral activity, increased activity. The ipsilateral AChT-positive cells in the injured ipsilateral vestibular system were decreased and the degree of bilateral reaction increased. Contralateral vestibular compensatory phase response increased significantly. In the acute phase, the ipsilateral NaKATP mRNA expression was low and the contralateral vestibular signal was enhanced. In the vestibular compensatory phase, the ipsilateral NaKATP mRNA expression was increased, consistent with or slightly stronger than contralateral. Conclusions The outgoing vestibular nervous system may inhibit the contralateral vestibular afferent information and adjust the excitability of the ipsilateral vestibular center, playing a role in the complex mechanism of vestibular compensation.