Intrinsic excitability changes in vestibular nucleus neurons after unilateral deafferentation
Intrinsic excitability changes in vestibular nucleus neurons after unilateral deafferentation
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DOI：
10.1016/s0006-8993(01)02600-2
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发表时间：
2001-07-20
期刊：
影响因子：
2.9
通讯作者：
Dutia, MB
中科院分区：
文献类型：
--
作者：
Him, A;Dutia, MB
最近在大鼠内侧前庭核(MVN)神经元中发现了两种协同可塑性机制，即前庭代偿，即一个内耳的前庭感受器或神经受损后的行为恢复。单侧前庭去传入后4h内，损毁的MVN神经元的内源性兴奋性显著增强，GABAA和GABA(B)受体的功能效能显著降低。这些机制可能抵消了去传入后损伤细胞的障碍和过度的连合抑制，从而促进了静息活动的恢复。在本研究中，我们研究了前庭代偿24-72小时和7-10天的动物脑片上嘴侧损毁的MVN神经元的固有膜特性和放电特性。B型细胞的自发放电率、静息膜电位和电压激活膜电导均有显著变化，而A型细胞则无明显变化。与正常相比，B-LTS细胞数量显著增加。这些结果表明，在前庭代偿过程中，B型MVN神经元的离子通道表达和功能发生了显着变化。这些变化适合于提高B型细胞对自身固有的起搏器样膜电导和兴奋性突触输入的反应性。再加上抑制性受体效应的下调，这种内在兴奋性的增加可能足以恢复体内去传入神经元的静息放电。因此，这些结果为前庭代偿过程中单侧MVN神经元的突触和神经元可塑性提供了进一步的证据。(C)2001年，爱思唯尔科学公司出版。
Two synergistic plastic mechanisms have recently been identified in rat medial vestibular nucleus (MVN) neurons during `vestibular compensation', the behavioral recovery that follows damage to the vestibular receptors or nerve of one inner ear. Ipsi-lesional MVN neurons develop a significant increase in their intrinsic excitability, and a marked decrease in the functional efficacy of GABAA and GABA(B) receptors, within 4 h of unilateral vestibular deafferentation. These mechanisms presumably counteract the disfacilitation and excessive commissural inhibition of the ipsi-lesional cells after deafferentation, and thus promote the recovery of resting activity. In this study, we investigated the intrinsic membrane properties and spike firing characteristics of rostral ipsi-lesional MVN neurons in slices from animals that underwent vestibular compensation for either 24-72 h or 7-10 days. Significant changes were observed in the spontaneous in vitro discharge rate, resting membrane potentials and voltage-activated membrane conductances of type B cells, but not type A cells. There was a significant increase in the number of type B-LTS cells compared to normal. These findings indicate that during vestibular compensation marked changes occur in ion channel expression and function selectively in type B MVN neurons. These changes are appropriate to increase the responsiveness of type B cells both to their own intrinsic pacemaker-like membrane conductances and excitatory synaptic inputs. Together with the downregulation of inhibitory receptor efficacy, this increased intrinsic excitability may be sufficient to restore the resting discharge of the deafferented neurons' in vivo. These results therefore provide further evidence for synaptic and neuronal plasticity in ipsi-lesional MVN neurons during vestibular compensation. (C) 2001 Published by Elsevier Science B.V.