首页> 美国卫生研究院文献>Frontiers in Neurology >Noise Trauma Induced Neural Plasticity Throughout the Auditory System of Mongolian Gerbils: Differences between Tinnitus Developing and Non-Developing Animals
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Noise Trauma Induced Neural Plasticity Throughout the Auditory System of Mongolian Gerbils: Differences between Tinnitus Developing and Non-Developing Animals

机译:噪声外伤引起蒙古沙鼠听觉系统的神经可塑性:发育中的和未发育中的动物耳鸣之间的差异

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摘要

In this study, we describe differences between neural plasticity in auditory cortex (AC) of animals that developed subjective tinnitus (group T) after noise-induced hearing loss (NIHL) compared to those that did not [group non-tinnitus (NT)]. To this end, our analysis focuses on the input activity of cortical neurons based on the temporal and spectral analysis of local field potential (LFP) recordings and an in-depth analysis of auditory brainstem responses (ABR) in the same animals. In response to NIHL in NT animals we find a significant general reduction in overall cortical activity and spectral power as well as changes in all ABR wave amplitudes as a function of loudness. In contrast, T-animals show no significant change in overall cortical activity as assessed by root mean square analysis of LFP amplitudes, but a specific increase in LFP spectral power and in the amplitude of ABR wave V reflecting activity in the inferior colliculus (IC). Based on these results, we put forward a refined model of tinnitus prevention after NIHL that acts via a top-down global (i.e., frequency-unspecific) inhibition reducing overall neuronal activity in AC and IC, thereby counteracting NIHL-induced bottom-up frequency-specific neuroplasticity suggested in current models of tinnitus development.
机译:在这项研究中,我们描述了噪声诱发的听力损失(NIHL)后出现主观性耳鸣(T组)的动物与没有听觉皮层(AC)的动物之间的神经可塑性之间的差异。 。为此,我们的分析集中在基于局部场电势(LFP)记录的时间和频谱分析以及对同一动物的听觉脑干反应(ABR)的深入分析基础上的皮质神经元的输入活动。针对NT动物中的NIHL,我们发现总体皮层活动和频谱功率以及所有ABR波振幅的变化都随着响度的变化而显着降低。相比之下,通过对LFP振幅的均方根分析评估,T动物的总体皮层活动没有显着变化,但是LFP光谱功率和反映下丘(IC)活动的ABR波V振幅有特定的增加。基于这些结果,我们提出了一种完善的NIHL后耳鸣预防模型,该模型通过自上而下的全局(即频率非特异性)抑制作用来降低AC和IC中的整体神经元活动,从而抵消了NIHL引起的自下而上的频率当前耳鸣发展模型中建议的特定神经可塑性。

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