EFFECTS OF MK801 ON FOS EXPRESSION IN THE RAT BRAIN-STEM AFTER UNILATERAL LABYRINTHECTOMY

被引：55

作者：

KITAHARA, T ^{[1
]}

TAKEDA, N ^{[1
]}

SAIKA, T ^{[1
]}

KUBO, T ^{[1
]}

KIYAMA, H ^{[1
]}

机构：

[1] OSAKA UNIV,SCH MED,DEPT NEUROANAT,SUITA,OSAKA 565,JAPAN

来源：

BRAIN RESEARCH | 1995年 / 700卷 / 1-2期

关键词：

VESTIBULAR COMPENSATION; NEURAL PLASTICITY; DECOMPENSATION; NNYSTAGMUS; N-METHYL-D-ASPARTATE RECEPTOR; IMMUNOHISTOCHEMISTRY;

D O I：

10.1016/0006-8993(95)00950-U

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Unilateral labyrinthectomy (UL) causes ocular and postural asymmetries, which disappear over time in the processes of equilibrium recovery known as vestibular compensation. It has been reported that N-methyl-D-aspartate (NMDA) receptors are involved in vestibular compensation. In the present study, in order to elucidate the NMDA receptor-mediated neural circuit responsible for the development of vestibular compensation, we used Fos expression as a marker of neural activation and examined the effects of MK801, a specific antagonist of NMDA receptors, on UL-induced Fos expression in the rat brainstem. After UL, Fos-like immunoreactive (-LIR) neurons were observed in the ipsilateral medial vestibular nucleus (ipsi-MVe), the contralateral prepositus hypoglossal nucleus (contra-PrH) and the contralateral inferior olive beta subnucleus (contra-IOb). Fos-LIR neurons then gradually disappeared in the processes of vestibular compensation. It is suggested that the activation of the ipsi-MVe, the contra-PrH and the contra-IOb neurons after UL are the initial event of vestibular compensation. Intraperitoneal injection of MK801 in the processes of vestibular compensation caused reappearance of UL-induced behavioral deficits. During the decompensation induced by MK801, Fos-LIR neurons appeared in the contra-MVe, the ipsi-PrH and the bilateral-IOb. It is suggested that the contra-MVe, the ipsi-PrH and the bilateral-IOb neurons are inhibited by glutamatergic synapses driving inhibitory neurons via NMDA receptors in the processes of vestibular compensation and that disinhibition of these nuclei induced by MK801 causes decompensation. However, MK801 caused neither Fos expression nor behavioral decompensation after vestibular compensation is accomplished. All these findings suggest that the NMDA receptor-mediated inhibitory modulation in the central vestibular system plays an important role for the initial processes of the development of vestibular compensation.

引用

页码：182 / 190

页数：9

共 42 条

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