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Physiological and anatomical observations of the neural integrator in compensations of sensory organs

感觉器官补偿中神经积分器的生理和解剖学观察

基本信息

批准号：
17591786
负责人：
TSUJI Jun
金额：
$ 2.24万
依托单位：
Clinical Research Center, Kyoto Medical Center
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2005
资助国家：
日本
起止时间：
2005 至 2006
项目状态：
已结题

项目摘要

Vestibular compensation is attributed to functional and structural reorganization of neural networks in the central vestibular system, but its precise mechanism is still not clear. c-Fos protein is used as a marker of neuronal activation, because of its very limited expression in the normal state and rapid appearance after external stimulation. Previous reports, investigating c-Fos expression after unilateral labyrinthectomy were made in rats and guinea pigs, but not in the mouse brainstem. We elucidated, after unilateral labyrinthectomy in mice, the bilateral medial vestibular nucleus (MVe), bilateral spinal vestibular nucleus (SpVe), contralateral prepositus hypoglossal nucleus (PrH), and contralateral inferior olive nucleus (IO) were activated like in other species.It is well known that the fixating mechanism of visual system suppress nystagmus of vestibular origin(visual suppression). And it is generally assumed that floccular Purkinje cells encodes retinal slip and controls the gain of the horizontal vestibulo-ocular reflex. Previous reports showed that lesions in the flocculus abolish visual suppression. However the precise mechanism of the visual suppression is not completely understood. We recorded the visual suppressions in mutant mice deficient in the delta 2 subunit of the ionotrphhic glutamate receptor (GluR delta-2) in Purkinje cells to investigate the role of glutaminergic system on the control of VOR. Eye movements were captured and analyzed by a computer. The pupil was fitted as an ellipse and the horizontal eye angular movement was calculated using the shape and direction of ellipse (Iwashita et al. 2001). In GluR delta-2 (-/-)mice the velocity was reduced very little (10 %), no change or even increased in light. These results suggest that the parallel fiber input to floccular Purkinje cells mediated by ionotrophic glutamate receptor play important roles in the visual suppression of the vestibular nystagmus.

前庭代偿归因于前庭中枢神经网络的功能和结构重组，但其确切机制尚不清楚。C-Fos蛋白在正常状态下的表达非常有限，在外界刺激后迅速出现，因此被认为是神经元激活的标志。以前的报道，研究了大鼠和豚鼠单侧迷路切除后c-Fos的表达，但没有在小鼠脑干中进行。我们阐明，在小鼠一侧迷路切除后，双侧前庭内侧核(MVE)、双侧脊髓前庭核(SpVe)、对侧舌下前置核(PRH)和对侧下橄榄核(IO)像其他物种一样被激活。众所周知，视觉系统的固定机制抑制了前庭起源的眼球震颤(视觉抑制)。一般认为，绒毛状浦肯野细胞编码视网膜滑移，控制水平前庭-眼反射的获得。以前的报道表明，小叶中的病变可以消除视觉抑制。然而，视觉抑制的确切机制尚不完全清楚。我们记录了浦肯野细胞离子磷酸谷氨酸受体(GluR Delta-2)delta2亚单位缺陷突变小鼠的视觉抑制，以探讨谷氨酸能系统在VOR控制中的作用。眼球运动被计算机捕捉和分析。将瞳孔拟合成椭圆，并利用椭圆的形状和方向计算眼睛的水平角运动(Iwashita等人)。2001)。在Glur Delta-2(-/-)小鼠中，光的速度下降很少(10%)，没有变化甚至增加。这些结果提示，离子营养型谷氨酸受体介导的平行纤维传入小叶浦肯野细胞在前庭震颤的视觉抑制中起重要作用。