Loss of peripheral vestibular function provokes severe impairments of gaze and posture stabilization in humans and animals. However, relatively little is known about the extent of the instantaneous deficits. This is mostly due to the fact that in humans a spontaneous loss often goes unnoticed initially and targeted lesions in animals are performed under deep anesthesia, which prevents immediate evaluation of behavioral deficits. Here, we use isolated preparations of Xenopus laevis tadpoles with functionally intact vestibulo-ocular (VOR) and optokinetic reflexes (OKR) to evaluate the acute consequences of unilateral VIIIth nerve sections. Such in vitro preparations allow lesions to be performed in the absence of anesthetics with the advantage to instantly evaluate behavioral deficits. Eye movements, evoked by horizontal sinusoidal head/table rotation in darkness and in light, became reduced by 30% immediately after the lesion and were diminished by 50% at 1.5 h postlesion. In contrast, the sinusoidal horizontal OKR, evoked by large-field visual scene motion, remained unaltered instantaneously but was reduced by more than 50% from 1.5 h postlesion onwards. The further impairment of the VOR beyond the instantaneous effect, along with the delayed decrease of OKR performance, suggests that the immediate impact of the sensory loss is superseded by secondary consequences. These potentially involve homeostatic neuronal plasticity among shared VOR-OKR neuronal elements that are triggered by the ongoing asymmetric activity. Provided that this assumption is correct, a rehabilitative reduction of the vestibular asymmetry might restrict the extent of the secondary detrimental effect evoked by the principal peripheral impairment.

外周前庭功能的丧失会引起人和动物的凝视和姿势稳定的严重损害。但是，对瞬时缺陷程度的了解相对较少。这主要是由于这样的事实，即在人类中，最初自然不易注意到自发性损失，而在深度麻醉下对动物进行了针对性的损害，这阻止了对行为缺陷的立即评估。在这里，我们使用非洲爪蟾的分离制剂具有功能完整的前庭眼（VOR）和视动反射（OKR）的，以评估第VIII侧神经段的急性后果。这种体外制剂允许在不使用麻醉剂的情况下进行损害，其优点是可以立即评估行为缺陷。在黑暗和光线下，水平正弦形头部/工作台旋转引起的眼球运动在病变后立即减少30％，并在病变后1.5小时减少50％。相比之下，由大视野视觉场景运动引起的正弦水平OKR瞬时保持不变，但从病变1.5小时起降低了50％以上。VOR的进一步损害超出了即时影响，以及OKR性能的延迟下降，提示感觉丧失的直接影响已被次要后果所取代。这些可能涉及由持续的不对称活动触发的共享VOR-OKR神经元之间的稳态神经元可塑性。只要这个假设是正确的，修复前庭不对称性的减少可能会限制主要外周损伤引起的继发性有害作用的程度。