Presynaptic and postsynaptic ion channel expression in vestibular nuclei neurons after unilateral vestibular deafferentation.
Presynaptic and postsynaptic ion channel expression in vestibular nuclei neurons after unilateral vestibular deafferentation.
复制标题
DOI：
10.3233/ves-2009-0348
复制
发表时间：
2009
期刊：
影响因子：
--
通讯作者：
M. Shao;A. Popratiloff;J. Hirsch;K. Peusner
中科院分区：
文献类型：
--
作者：
M. Shao;A. Popratiloff;J. Hirsch;K. Peusner
前庭代偿是指单侧前庭传入阻滞后功能恢复，但仍有部分患者未恢复。同样，一半以上的手术鸡补偿单侧前庭神经节切除术（UVG）后三天，但其余的仍然没有补偿。本文综述了紫外线照射后鸡的切向核主细胞的研究进展。切向核是主要的鸟类前庭神经核，其主要细胞都是二级前庭反射投射神经元，参与控制姿势、平衡和眼球运动的前庭眼反射和前庭颈反射。在脑切片制备中使用全细胞膜片钳方法，在UVG后三天记录对照和手术鸡的主细胞中的自发尖峰放电、离子电导和自发兴奋性突触后电流（sEPSC）。在代偿期，病变侧和正常侧自发锋电位放电主细胞的比例和锋电位放电率均呈对称性，且均高于对照组。然而，在未补偿的鸡，尖峰放电率增加的病变侧，但不是在完整的一面，只有沉默的主细胞记录。在所有实验组中，包括对照组，沉默的主细胞区分自发尖峰细胞较小的持续钠电导和较高的激活阈值的快钠通道。此外，沉默的主细胞上的完整的一面无补偿鸡有较大的树突状毒素敏感的钾电导，与较高的比率的树突状毒素敏感的，钾通道亚基，Kv1.1的表面/细胞质表达的免疫标记。最后，在补偿鸡，sEPSC的频率是对称的双边，但在未补偿鸡sEPSC的频率增加，只在病变侧，其中Kv1.2的表达减少在突触结合蛋白标记的终端配置文件的主要细胞体。总而言之，特定的钠和钾通道重要的发展的尖峰放电模式和/或突触前谷氨酸释放的前庭反射投射神经元可能是至关重要的参与改变前庭传入神经阻滞后突触后神经元兴奋性。
Vestibular compensation refers to the recovery of function occurring after unilateral vestibular deafferentation, but some patients remain uncompensated. Similarly, more than half of the operated chickens compensate three days after unilateral vestibular ganglionectomy (UVG), but the rest remain uncompensated. This review focuses on the studies performed on the principal cells of the chick tangential nucleus after UVG. The tangential nucleus is a major avian vestibular nucleus whose principal cells are all second-order, vestibular reflex projection neurons participating in the vestibuloocular and vestibulocollic reflexes controlling posture, balance, and eye movements. Using whole-cell patch-clamp approach in brain slice preparations, spontaneous spike firing, ionic conductances, and spontaneous excitatory postsynaptic currents (sEPSCs) are recorded in principal cells from controls and operated chickens three days after UVG. In compensated chickens, the proportion of spontaneous spike firing principal cells and their spike discharge rate are symmetric on the lesion and intact sides, with the rates increased over controls. However, in the uncompensated chickens, the spike discharge rate increases on the lesion side, but not on the intact side, where only silent principal cells are recorded. In all the experimental groups, including controls, silent principal cells are distinguished from spontaneous spiking cells by smaller persistent sodium conductances and higher activation thresholds for the fast sodium channel. In addition, silent principal cells on the intact side of uncompensated chickens have larger dendrotoxin-sensitive potassium conductances, with a higher ratio of immunolabeling for surface/cytoplasmic expression of a dendrotoxin-sensitive, potassium channel subunit, Kv1.1. Finally, in compensated chickens, sEPSC frequency is symmetric bilaterally, but in uncompensated chickens sEPSC frequency increased only on the lesion side, where the expression of Kv1.2 decreased in synaptotagmin-labeled terminal profiles on the principal cell bodies. Altogether, the specific sodium and potassium channels important for the development of spike firing pattern and/or presynaptic glutamate release on vestibular reflex projection neurons may be critically involved in changing postsynaptic neuron excitability after vestibular deafferentation.