Neural Mechanisms of Vestibular Compensation and Development of Drugs for Facilitating the Processes of Vestibular Compensation

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  • 前庭代償の神経メカニズムの解明と前庭代償促進薬の開発
  • ゼンテイ ダイショウ ノ シンケイ メカニズム ノ カイメイ ト ゼンテイ ダイショウ ソクシンヤク ノ カイハツ

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Abstract

<p>Unilateral vestibular dysfunction causes spontaneous nystagmus (SN) and deviations of posture and locomotion. However, the nystagmus and imbalance eventually recover gradually; this functional restoration based on the plasticity of the central vestibular system is called vestibular compensation (VC). VC is divided into static and dynamic VC. Static VC is further subdivided into initial and late processes. In the initial process, the neural activities of the contralateral medial vestibular nucleus (contra-MVe) are inhibited by the cerebello-vestibular inhibitory pathway, and in the late process, the neural activities of the ipsilateral medial vestibular nucleus (ipsi-MVe) are restored after unilateral labyrinthectomy (UL). The initial process of VC was evaluated by observing the decline of the frequency of SN after UL in rats. Diazepam, a GABAA receptor agonist, facilitated the disappearance of SN after UL in rats, suggesting that the GABAA agonist facilitated the initial process of VC. We then developed a new immunohistochemical method to evaluate the late process of VC in the rats after UL, and showed that the late process of VC can be demonstrated by the decline in the number of MK801 (an NMDA receptor antagonist)-induced Fos-positive neurons in the contra-MVe after UL. Thioperamide or betahistine, which are histamine H3 receptor antagonists, facilitated the disappearance of MK801-induced Fos-positive neurons in the contra-Mve after UL in the rats, suggesting that histamine H3 antagonists facilitate the late process of VC.</p>

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