Southern Connecticut State University, New Haven, Connecticut.
J Neurosci Res. 2012 Apr;90(4):831-41. doi: 10.1002/jnr.22793. Epub 2011 Nov 23.
To study the mechanisms of noise-induced hearing loss and the phantom noise, or tinnitus, often associated with it, we used a mouse model of noise damage designed for reproducible and quantitative structural analyses. We selected the posteroventral cochlear nucleus, which has shown considerable plasticity in past studies, and correlated its changes with the distribution of neurotrophin 3 (NT3). We used volume change, optical density analysis, and microscopic cluster analysis to measure the degeneration after noise exposure. There was a fluctuation pattern in the reorganization of nerve terminals. The data suggest that the source and size of the nerve terminals affect their capacity for regeneration. We hypothesize that the deafferentation of ventral cochlear nucleus is the structural basis of noise-induced tinnitus. In addition, the immunofluorescent data show a possible connection between NT3 and astrocytes. There appears to be a compensatory process in the supporting glial cells during this degeneration. Glia may play a role in the mechanisms of noise-induced hearing loss.
为了研究噪声性听力损失的机制以及与之相关的幻听(耳鸣),我们使用了一种为可重复性和定量结构分析而设计的噪声损伤小鼠模型。我们选择了后腹耳蜗核,在过去的研究中它显示出了相当大的可塑性,并将其变化与神经营养因子 3(NT3)的分布相关联。我们使用体积变化、光密度分析和微观聚类分析来测量噪声暴露后的退化。神经末梢的重组呈现出波动模式。数据表明,神经末梢的来源和大小影响其再生能力。我们假设,耳蜗腹核的去传入是噪声性耳鸣的结构基础。此外,免疫荧光数据显示 NT3 与星形胶质细胞之间可能存在联系。在这种退化过程中,支持性胶质细胞似乎存在一种代偿过程。胶质细胞可能在噪声性听力损失的机制中发挥作用。