Glutamatergic and GABAergic neurons represent the neural components of the medial vestibular nuclei. We assessed the functional role of glutamatergic and GABAergic neuronal pathways arising from the vestibular nuclei (VN) in the maintenance of gait and balance by optogenetically stimulating the VN in VGluT2-cre and GAD2-cre mice. We demonstrate that glutamatergic, but not GABAergic VN neuronal subpopulation is responsible for immediate and strong posturo-locomotor deficits, comparable to unilateral vestibular deafferentation models. During optogenetic stimulation, the support surface dramatically increased in VN^VGluT2+ mice, and rapidly fell back to baseline after stimulation, whilst it remained unchanged during similar stimulation of VN^GAD2+ mice. This effect persisted when vestibular tactilo kinesthesic plantar inputs were removed. Posturo-locomotor alterations evoked in VN^VGluT2+ animals were still present immediately after stimulation, while they disappeared 1 h later. Overall, these results indicate a fundamental role for VN^VGluT2+ neurons in balance and posturo-locomotor functions, but not for VN^GAD2+ neurons, in this specific context. This new optogenetic approach will be useful to characterize the role of the different VN neuronal populations involved in vestibular physiology and pathophysiology.

谷氨酸能和 GABA 能神经元代表内侧前庭核的神经成分。我们通过光遗传学刺激 VGluT2-cre 和 GAD2-cre 小鼠中的 VN，评估了由前庭核 (VN) 产生的谷氨酸能和 GABA 能神经元通路在维持步态和平衡中的功能作用。我们证明谷氨酸能，但不是 GABAergic VN 神经元亚群是造成立即和强烈的后运动缺陷的原因，与单侧前庭传入神经阻滞模型相当。^{在光遗传学刺激期间，VN VGluT2+}小鼠的支持表面显着增加，并在刺激后迅速回落到基线，而在类似的 VN ^{GAD2+刺激期间它保持不变}老鼠。当去除前庭触觉动觉足底输入时，这种效果仍然存在。在 VN ^VGluT2+动物中诱发的姿势运动改变在刺激后立即仍然存在，而它们在 1 小时后消失。总体而言，这些结果表明 VN ^VGluT2+神经元在平衡和后运动功能中的基本作用，但不是 VN ^GAD2+神经元，在这个特定的背景下。这种新的光遗传学方法将有助于表征参与前庭生理学和病理生理学的不同 VN 神经元群体的作用。