Department of Physiology, University of Arizona College of Medicine, Tucson, AZ, 85724, USA.
Sci Rep. 2020 Nov 24;10(1):20445. doi: 10.1038/s41598-020-75714-1.
Exposure to loud noises results in neuroinflammatory responses in the central auditory pathway. Noise-induced neuroinflammation is implicated in auditory processing deficits such as impairment in gap detection. In this study, we examined whether strain differences between the FVB and C57BL/6 mice in noise-induced impairment in gap detection are correlated with strain differences in neuroinflammatory responses. We found that noise induced more robust TNF-α expression in C57BL/6 than in FVB mice. Noise-induced microglial deramification was observed in C57BL/6 mice, but not in FVB mice. Furthermore, noise exposure resulted in a reduction in parvalbumin-positive (PV+) neuron density in the C57BL/6 mice, but not in FVB mice. These results suggest that neuroinflammatory responses and loss of PV+ neurons may contribute to strain differences in noise-induced impairment in gap detection.
暴露于大声噪声会导致中枢听觉通路中的神经炎症反应。噪声引起的神经炎症与听觉处理缺陷有关,例如缝隙检测受损。在这项研究中,我们研究了 FVB 和 C57BL/6 小鼠之间在噪声引起的缝隙检测损伤中的应变差异是否与神经炎症反应中的应变差异相关。我们发现,与 FVB 小鼠相比,噪声在 C57BL/6 小鼠中诱导了更强烈的 TNF-α表达。在 C57BL/6 小鼠中观察到了噪声诱导的小胶质细胞变形,但在 FVB 小鼠中没有观察到。此外,噪声暴露导致 C57BL/6 小鼠中 PV+神经元密度减少,但在 FVB 小鼠中没有。这些结果表明,神经炎症反应和 PV+神经元的丧失可能导致在噪声引起的缝隙检测损伤中的应变差异。