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小鼠内侧膝状体和初级听觉皮层因声学过度刺激导致细胞死亡的时间进程。

Time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex.

作者信息

Frohlich Felix, Basta Dietmar, Strübing Ira, Ernst Arne, Gröschel Moritz

机构信息

Department of Otolaryngology, Unfallkrankenhaus Berlin, Charité Medical School, Warener Straße 7, Berlin, Germany.

出版信息

Noise Health. 2017 May-Jun;19(88):133-139. doi: 10.4103/nah.NAH_10_17.

DOI:10.4103/nah.NAH_10_17
PMID:28615543
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5501023/
Abstract

It has previously been shown that acoustic overstimulation induces cell death and extensive cell loss in key structures of the central auditory pathway. A correlation between noise-induced apoptosis and cell loss was hypothesized for the cochlear nucleus and colliculus inferior. To determine the role of cell death in noise-induced cell loss in thalamic and cortical structures, the present mouse study (NMRI strain) describes the time course following noise exposure of cell death mechanisms for the ventral medial geniculate body (vMGB), medial MGB (mMGB), and dorsal MGB (dMGB) and the six histological layers of the primary auditory cortex (AI 1-6). Therefore, a terminal deoxynucleotidyl transferase dioxyuridine triphosphate nick-end labeling assay (TUNEL) was performed in these structures 24 h, 7 days, and 14 days after noise exposure (3 h, 115 dB sound pressure level, 5-20 kHz), as well as in unexposed controls. In the dMGB, TUNEL was statistically significant elevated 24 h postexposure. AI-1 showed a decrease in TUNEL after 14 days. There was no statistically significant difference between groups for the other brain areas investigated. dMGB's widespread connection within the central auditory pathway and its nontonotopical organization might explain its prominent increase in TUNEL compared to the other MGB subdivisions and the AI. It is assumed that the onset and peak of noise-induced cell death is delayed in higher areas of the central auditory pathway and takes place between 24 h and 7 days postexposure in thalamic and cortical structures.

摘要

先前的研究表明,声学过度刺激会导致中枢听觉通路关键结构中的细胞死亡和大量细胞损失。有人推测,噪声诱导的细胞凋亡与耳蜗核和下丘的细胞损失之间存在关联。为了确定细胞死亡在丘脑和皮质结构的噪声诱导细胞损失中的作用,本小鼠研究(NMRI品系)描述了噪声暴露后腹内侧膝状体(vMGB)、内侧膝状体(mMGB)和背侧膝状体(dMGB)以及初级听觉皮层(AI 1-6)的六个组织学层的细胞死亡机制的时间进程。因此,在噪声暴露(3小时,115分贝声压级,5-20千赫)后24小时、7天和14天,以及在未暴露的对照组中,对这些结构进行了末端脱氧核苷酸转移酶介导的缺口末端标记测定(TUNEL)。在dMGB中,暴露后24小时TUNEL有统计学意义的升高。AI-1在14天后TUNEL有所下降。在所研究的其他脑区,各组之间没有统计学意义的差异。dMGB在中枢听觉通路内广泛的连接及其非拓扑组织可能解释了与其他MGB细分区域和AI相比,其TUNEL的显著增加。据推测,噪声诱导的细胞死亡的起始和峰值在中枢听觉通路的较高区域延迟,并且在丘脑和皮质结构中暴露后24小时至7天之间发生。

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Immediate manifestation of acoustic trauma in the auditory cortex is layer specific and cell type dependent.听觉皮层中声创伤的即时表现具有层特异性和细胞类型依赖性。
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