Kitahara T, Takeda N, Saika T, Kubo T, Kiyama H
Department of Neuroanatomy, Osaka University Medical School, Suita, Japan.
Neuroscience. 1997 Jan;76(2):571-80. doi: 10.1016/s0306-4522(96)00374-0.
After unilateral labyrinthectomy in rats, Fos-like immunoreactive neurons appeared in the ipsilateral medial vestibular nucleus, contralateral prepositus hypoglossal nucleus and contralateral inferior olive beta subnucleus. and thereafter gradually disappeared in accordance with the development of vestibular compensation. This finding indicated that the activation of these nuclei is the initial event of vestibular compensation. In the present study, retrograde tracing experiments revealed that these Fos-like immunoreactive neurons project a proportion of their axons to the vestibulocerebellum (uvula-nodulus, flocculus). Before vestibular compensation was accomplished, right, left or bilateral flocculectomy was performed in right-labyrinthectomized rats. All these treatments caused reappearance of unilateral labyrinthectomy-induced behavioral deficits and Fos expression in the left medial vestibular nucleus and right prepositus hypoglossal nucleus. Since floccular efferents are GABAergic, these results indicate that the neurons in which Fos expression was detected by flocculectomy had been inhibited after unilateral labyrinthectomy by floccular Purkinje neurons and that disinhibition of these neurons induced by flocculectomy caused decompensation. Based on our present findings, we propose a hypothesis that the bilateral flocculus serves the restoration of balance between intervestibular nuclear activities to induce vestibular compensation after unilateral labyrinthectomy.
大鼠单侧迷路切除术后,Fos样免疫反应性神经元出现在同侧内侧前庭核、对侧舌下前置核和对侧下橄榄β亚核,并随后随着前庭代偿的发展逐渐消失。这一发现表明这些核的激活是前庭代偿的初始事件。在本研究中,逆行追踪实验显示,这些Fos样免疫反应性神经元将其一部分轴突投射到前庭小脑(蚓垂-小结、绒球)。在前庭代偿完成之前,对右侧迷路切除的大鼠进行右侧、左侧或双侧绒球切除。所有这些处理均导致单侧迷路切除引起的行为缺陷再次出现,以及左侧内侧前庭核和右侧舌下前置核中Fos表达增加。由于绒球传出纤维是γ-氨基丁酸能的,这些结果表明,在单侧迷路切除术后,绒球浦肯野神经元抑制了通过绒球切除检测到Fos表达的神经元,而绒球切除引起的这些神经元的去抑制导致了失代偿。基于我们目前的发现,我们提出一个假说,即双侧绒球在单侧迷路切除术后通过恢复前庭核间活动的平衡来诱导前庭代偿。