Central Compensation in Auditory Brainstem after Damaging Noise Exposure.
Central Compensation in Auditory Brainstem after Damaging Noise Exposure.
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DOI：
10.1523/eneuro.0250-18.2018
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发表时间：
2018-07
期刊：
影响因子：
3.4
通讯作者：
Lauer AM
中科院分区：
文献类型：
--
作者：
Schrode KM;Muniak MA;Kim YH;Lauer AM
噪声暴露是听力损失和听觉系统外围损伤的最常见原因之一。越来越多的文献表明，听觉系统可以通过增加中枢神经活动来补偿外周损失。目前的研究试图调查噪声暴露，增加中枢增益，突触重组和听觉功能之间的联系。听觉神经的所有轴突都投射到耳蜗核，使其成为声音检测的必要核。耳蜗核作为中枢听觉系统的第一个突触，对外周输入的丧失具有可塑性反应。为了研究噪声引起的中枢听觉系统的补偿，我们测量了听觉脑干反应（ABR）和听觉感知，并收集了暴露于宽带噪声的小鼠的组织。噪声暴露的小鼠表现出ABR阈值升高，ABR波1振幅降低，螺旋神经节神经元丢失。尽管外周损伤，噪声暴露的小鼠对响亮的声音反应过度，表现出接近正常的行为声音检测阈值。晚期ABR峰（2-4）相对于第一个ABR峰的比率表明，噪声暴露小鼠的脑干通路过度活跃，而解剖学分析表明，耳蜗腹侧核中兴奋性和抑制性蛋白的表达之间存在不平衡。目前的研究结果表明，耳蜗腹侧核的兴奋和抑制的重组可能会驱动中枢听觉系统的过度活跃。这种中枢增益的增加可以补偿外周损失，以恢复听觉功能的某些方面。
Noise exposure is one of the most common causes of hearing loss and peripheral damage to the auditory system. A growing literature suggests that the auditory system can compensate for peripheral loss through increased central neural activity. The current study sought to investigate the link between noise exposure, increases in central gain, synaptic reorganization, and auditory function. All axons of the auditory nerve project to the cochlear nucleus, making it a requisite nucleus for sound detection. As the first synapse in the central auditory system, the cochlear nucleus is well positioned to respond plastically to loss of peripheral input. To investigate noise-induced compensation in the central auditory system, we measured auditory brainstem responses (ABRs) and auditory perception and collected tissue from mice exposed to broadband noise. Noise-exposed mice showed elevated ABR thresholds, reduced ABR wave 1 amplitudes, and spiral ganglion neuron loss. Despite peripheral damage, noise-exposed mice were hyperreactive to loud sounds and showed nearly normal behavioral sound detection thresholds. Ratios of late ABR peaks (2–4) relative to the first ABR peak indicated that brainstem pathways were hyperactive in noise-exposed mice, while anatomical analysis indicated there was an imbalance between expression of excitatory and inhibitory proteins in the ventral cochlear nucleus. The results of the current study suggest that a reorganization of excitation and inhibition in the ventral cochlear nucleus may drive hyperactivity in the central auditory system. This increase in central gain can compensate for peripheral loss to restore some aspects of auditory function.