Rabbath G, Necchi D, de Waele C, Gasc J P, Josset P, Vidal P P
Laboratoire de Neurobiologie des Réseaux Sensorimoteurs, ESA 7060 (CNRS-Paris 5-Paris 7), France.
Exp Brain Res. 2001 Jan;136(2):211-23. doi: 10.1007/s002210000568.
The waltzing behavior is usually attributed to vestibular dysfunction. However, the vestibular control of gaze and posture has not yet been measured quantitatively in any waltzing mutant. Therefore, this study was aimed at investigating the relationship between inner-ear morphology, the circling behavior, and the vestibular control of gaze and posture in a new strain of waltzing rats. Light- and electron-microscopy studies of these mutants did not reveal any structural abnormalities of the vestibular neural epithelia. In addition, the expression of Calretinin and 200-kD phosphorylated and non-phosphorylated neurofilaments was also found to be normal in the vestibular neural epithelia and ganglion cells. In contrast, the mutants showed severe dysfunctions of the vestibular control of gaze and posture. The skeletal geometry of the alert unrestrained animals was studied using cineradiography. At rest, waltzing rats held their heads tilted down: the horizontal semicircular-canal's plane was near the earth-horizontal's plane, instead of being tilted up as in Long Evans control rats. In addition, their cervical column was pitched more forward (33.6 degrees) than in the control group (6.9 degrees). The circling behavior was observed frequently, and the rats had episodes of circling in both directions. The episodes of circling amounted to an average of 17 turns, and the average angular velocity of the circling was 645 degrees/s. Unilateral labyrinthectomy induced the same postural and oculomotor syndromes in the waltzing and control groups. This indicates that the mutant vestibular nerve had a significant resting discharge before the lesion. Eye movements were recorded using acutely implanted search coils. Although waltzing rats were able to perform normal spontaneous eye movements, they showed a complete deficit of the horizontal vestibulo-ocular reflex (HVOR) and an impairment of the maculo-ocular reflex (MOR) during constant velocity, off-vertical axis rotation (OVAR). These results show, for the first time, that deficient transduction and/or processing of the horizontal-canal- and macular-related information can be causally related to the circling behavior and abnormal posture, respectively.
旋转行为通常归因于前庭功能障碍。然而，在任何旋转突变体中，尚未对前庭对眼球运动和姿势的控制进行定量测量。因此，本研究旨在调查一种新的旋转大鼠品系的内耳形态、转圈行为以及前庭对眼球运动和姿势控制之间的关系。对这些突变体进行的光学显微镜和电子显微镜研究未发现前庭神经上皮有任何结构异常。此外，还发现钙视网膜蛋白以及200-kD磷酸化和非磷酸化神经丝在前庭神经上皮和神经节细胞中的表达也正常。相比之下，突变体在前庭对眼球运动和姿势的控制方面表现出严重功能障碍。使用电影X线摄影术研究了警觉不受约束动物的骨骼几何结构。在静止状态下，旋转大鼠头部向下倾斜：水平半规管平面接近地球水平面，而不是像朗·埃文斯对照大鼠那样向上倾斜。此外，它们的颈椎比对照组更向前倾斜（33.6度）（对照组为6.9度）。经常观察到转圈行为，大鼠会出现双向转圈发作。转圈发作平均为17圈，转圈的平均角速度为645度/秒。单侧迷路切除术在旋转组和对照组中诱发了相同的姿势和动眼综合征。这表明突变体前庭神经在损伤前有明显的静息放电。使用急性植入的搜索线圈记录眼球运动。尽管旋转大鼠能够进行正常的自发眼球运动，但在等速、离垂直轴旋转（OVAR）过程中，它们表现出完全缺乏水平前庭眼反射（HVOR）以及黄斑眼反射（MOR）受损。这些结果首次表明，水平半规管和黄斑相关信息的转导和/或处理缺陷可能分别与转圈行为和异常姿势存在因果关系。
