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前庭代偿过程中GABA(A)和GABA(B)受体的差异调节

Differential regulation of GABA(A) and GABA(B) receptors during vestibular compensation.

作者信息

Johnston A R, Him A, Dutia M B

机构信息

Department of Biomedical Sciences (Physiology), University of Edinburgh Medical School, UK.

出版信息

Neuroreport. 2001 Mar 5;12(3):597-600. doi: 10.1097/00001756-200103050-00033.

DOI:10.1097/00001756-200103050-00033
PMID:11234771
Abstract

We investigated changes in intrinsic excitability and GABA receptor efficacy in rat medial vestibular nucleus (MVN) neurons following 48 h and 7-10 days of behavioral recovery after unilateral labyrinthectomy (UL) in the rat. The mean in vitro discharge rate of rostral ipsilesional MVN cells at both time points was significantly higher than normal, indicating that the intrinsic excitability of the deafferented cells undergoes a sustained up-regulation during vestibular compensation. In slices from animals that had compensated for 7-10 days after UL, the responsiveness of rostral ipsilesional MVN cells to the GABA(A) agonist muscimol was not different from normal, while the responsiveness to the GABA(B) agonist baclofen was significantly down-regulated. This is in contrast to the situation soon after UL, where the efficacy of both GABA(A) and GABA(B) receptors is markedly down-regulated. The recovery of fast GABA(A) mediated neurotransmission by 7-10 days post-UL presumably enables ipsilesional cells to again respond to vestibular stimulation, through commissural inhibitory modulation from the intact side. The permanent loss of excitatory input from the lesioned side may be, in effect, counteracted by the long-term down-regulation of slow GABA(B) receptors in the de-afferented neurons.

摘要

我们研究了大鼠单侧迷路切除术后(UL)48小时以及行为恢复7 - 10天后,大鼠内侧前庭核(MVN)神经元的内在兴奋性和GABA受体效能的变化。在这两个时间点,吻侧同侧MVN细胞的平均体外放电率均显著高于正常水平,这表明在前庭代偿过程中,去传入神经细胞的内在兴奋性经历了持续上调。在UL后已代偿7 - 10天的动物切片中,吻侧同侧MVN细胞对GABA(A)激动剂蝇蕈醇的反应性与正常无异,而对GABA(B)激动剂巴氯芬的反应性则显著下调。这与UL后不久的情况相反,那时GABA(A)和GABA(B)受体的效能均显著下调。UL后7 - 10天快速GABA(A)介导的神经传递的恢复,大概使同侧细胞能够通过来自完整侧的连合抑制调节,再次对前庭刺激做出反应。损伤侧兴奋性输入的永久丧失,实际上可能会被去传入神经神经元中缓慢GABA(B)受体的长期下调所抵消。

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