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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >BDNF Signaling Promotes Vestibular Compensation by Increasing Neurogenesis and Remodeling the Expression of Potassium-Chloride Cotransporter KCC2 and GABA(A) Receptor in the Vestibular Nuclei
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BDNF Signaling Promotes Vestibular Compensation by Increasing Neurogenesis and Remodeling the Expression of Potassium-Chloride Cotransporter KCC2 and GABA(A) Receptor in the Vestibular Nuclei

机译：BDNF信号传导通过增加神经发生并重塑前庭核中氯化钾共转运蛋白KCC2和GABA（A）受体的表达来促进前庭补偿。

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摘要

Reactive cell proliferation occurs rapidly in the cat vestibular nuclei (VN) after unilateral vestibular neurectomy (UVN) and has been reported to facilitate the recovery of posturo-locomotor functions. Interestingly, whereas animals experience impairments for several weeks, extraordinary plasticity mechanisms take place in the local microenvironment of the VN: newborn cells survive and acquire different phenotypes, such as microglia, astrocytes, or GABAergic neurons, whereas animals eventually recover completely from their lesion-induced deficits. Because brain-derived neurotrophic factor (BDNF) can modulate vestibular functional recovery and neurogenesis in mammals, in this study, we examined the effect of BDNF chronic intracerebroventricular infusion versus K252a (a Trk receptor antagonist) in our UVN model. Results showed that long-term intracerebroventricular infusion of BDNF accelerated the restoration of vestibular functions and significantly increased UVN-induced neurogenesis, whereas K252a blocked that effect and drastically delayed and prevented the complete restoration of vestibular functions. Further, because the level of excitability in the deafferented VN is correlated with behavioral recovery, we examined the state of neuronal excitability using two specific markers: the cation-chloride cotransporter KCC2 (which determines the hyperpolarizing action of GABA) and GABA(A) receptors. We report for the first time that, during an early time window after UVN, significant BDNF-dependent remodeling of excitability markers occurs in the brainstem. These data suggest that GABA acquires a transient depolarizing action during recovery from UVN, which potentiates the observed reactive neurogenesis and accelerates vestibular functional recovery. These findings suggest that BDNF and/or KCC2 could represent novel treatment strategies for vestibular pathologies.
机译：反应性细胞增殖在单侧前庭神经切除术（UVN）后在猫前庭核（VN）中迅速发生，据报道可促进尿路后运动功能的恢复。有趣的是，尽管动物经历了数周的损伤，但在VN的局部微环境中却发生了异常的可塑性机制：新生细胞存活并获得了不同的表型，例如小胶质细胞，星形胶质细胞或GABA能神经元，而动物最终却从其病变中完全恢复了。导致赤字。因为脑源性神经营养因子（BDNF）可以调节哺乳动物的前庭功能恢复和神经发生，所以在这项研究中，我们在UVN模型中研究了BDNF慢性脑室内灌注与K252a（一种Trk受体拮抗剂）的关系。结果显示，长期脑室内注入BDNF可以加速前庭功能的恢复，并显着增加UVN诱导的神经发生，而K252a则可阻断该作用并大大延迟并阻止前庭功能的完全恢复。此外，因为脱去力的VN中的兴奋性水平与行为恢复相关，所以我们使用两个特定的标志物检查了神经元兴奋性的状态：阳离子-氯化物共转运蛋白KCC2（决定GABA的超极化作用）和GABA（A）受体。我们首次报告，在UVN后的早期时间窗内，脑干中发生了明显的BDNF依赖性兴奋性标志物重塑。这些数据表明，GABA在从UVN恢复过程中获得了短暂的去极化作用，从而增强了观察到的反应性神经发生并加速了前庭功能的恢复。这些发现表明，BDNF和/或KCC2可以代表前庭病理的新治疗策略。

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