Morphological and functional investigation of vestibular compensation

前庭代偿是前庭中枢神经网络功能和结构重组的结果，但其确切机制尚不清楚。即早基因c-Fos由于其在正常状态下表达非常有限且在刺激后迅速出现而被用作神经元激活的标志物。以前的研究报告，c-Fos表达后，单侧脑干切除大鼠和豚鼠，但没有在小鼠脑干。为了将来应用于基因敲除小鼠，我们研究了单侧睾丸切除术后小鼠中c-Fos的表达。术后24 h，双侧前庭内侧核（Mve）、前庭脊髓核（SpVe）和对侧舌下神经前置核（PrH）c-Fos阳性细胞数最多。在下橄榄核（IO），c-Fos阳性细胞在完整侧明显增多。我们的结果表明PrH核 ...更多信息 r细胞被激活，并且可以修改神经积分器。视觉系统的注视机制影响前庭源性眼球震颤，这是众所周知的。在黑暗中由热刺激引起的眼球震颤在光照下减少（视觉抑制）。一般认为，絮状浦肯野细胞编码视网膜滑移，并控制水平前庭眼反射的增益。先前的报告显示，在小叶病变取消视觉抑制。然而，视觉抑制的确切机制尚未完全了解。在本研究中，我们记录了浦肯野细胞离子型谷氨酸受体δ 2亚单位（GluR δ 2）缺陷突变小鼠的视觉抑制，以探讨多巴胺能系统在VOR控制中的作用。使用6-10周龄的野生型和纯合突变小鼠GluR delta-2（-/-）。左眼由红外LED照明，并由红外CCD相机监测。眼球运动被计算机捕捉和分析。将瞳孔拟合为椭圆，并使用椭圆的形状和方向计算水平眼角运动（Iwashita等人，2001）。通过在黑暗和光照下向左外耳道注射5 ml冰水进行热刺激。在野生型中，黑暗中的慢相速度在光照下降低约90%。在GluR delta-2（-/-）小鼠中，速度降低非常小（10%），在光照下没有变化甚至增加。这些结果提示，由谷氨酸离子型受体介导的对絮状浦肯野细胞的平行纤维输入在前庭性眼震的视觉抑制中起重要作用。少

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. Immediate early gene c-Fos is used as a marker of neuronal activation, because of its very limited expression in the normal state and quick appearance after stimulation. Previous reports, investigating c-Fos expression after unilateral labyrinthectomy were made in rats and guinea pigs, but not in the mouse brainstem. For future application to the gene knockout mouse, we examined c-Fos expression in the mouse after unilateral labyrinthectomy. Twenty-four hours after surgery, a highest number of c-Fos positive cells were observed in the bilateral medial vestibular nucleus (Mve), spinal vestibular nucleus (SpVe) and in the contra lateral prepositus hypoglossal nucleus (PrH). In the inferior olive nucleus (IO), c-Fos positive cells were significantly higher in the intact side. Our results suggest that PrH nuclea … More r cells are activated., and the neural integrator might be modified. in vestibular compensation period, thus adjust the VOR gains.It is well known that the fixating mechanism of visual system influences nystagmus of vestibular origin. Nystagmus induced by caloric stimulation in dark is reduced in light (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. In the present study, 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. Wild type and homozygous mutant mice GluR delta-2(-/-) 6-10 week old were used. The left eye was illuminated by an infrared LED and monitored by an infrared CCD camera. 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). Caloric stimulation was made by injection of 5-ml ice cold water into the left external ear canal in dark and light. In wild type the slow phase velocity in dark was reduced about 90 % in light. 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. Less