Exposure to short-lasting impulse noise causes neuronal c-Jun expression and induction of apoptosis in the adult rat brain
Exposure to short-lasting impulse noise causes neuronal c-Jun expression and induction of apoptosis in the adult rat brain
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DOI：
10.1089/089771502320317131
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发表时间：
2002-08-01
影响因子：
4.2
通讯作者：
Haglid, KG
中科院分区：
文献类型：
--
作者：
Säljö, A;Bao, F;Haglid, KG
暴露于一定强度以上的脉冲噪声中对听觉功能有害。脉冲噪声对中枢神经系统（CNS）的影响在很大程度上是未开发的，并且几乎没有关于临界阈值和时间因素的信息。我们最近发现，神经丝蛋白在大脑皮层和海马受到影响。现在，我们表明，脉冲噪声诱导表达的立即早期基因c-Jun的产品，提出发挥作用的神经元死亡的启动，和凋亡所揭示的TUNEL染色。本文对暴露于198 dB或202 dB脉冲噪声后2 h至21 d的大鼠脑组织进行了电化学研究。c-Jun在两种暴露水平后2 h至21 d在颞叶皮质、扣带回和梨状皮质的II-VI层神经元胞体中表达。齿状回的颗粒神经元和海马锥体神经元中的CA 1 -3也受到类似的影响。c-Jun产物的升高表达在所有的暴露后时间都保持高水平。TUNEL染色是阳性的相同的神经细胞群暴露后6小时，并持续到7天，甚至在两个曝光水平。
Exposure to impulse noise, above a certain intensity, is harmful to auditory function. Effects of impulse noise on the central nervous system (CNS) are largely unexplored, and there is little information on critical threshold values and time factors. We have recently shown that neurofilament proteins are affected in the cerebral cortex and the hippocampus. Now we show that impulse noise induces expression of the immediate early gene c-Jun products, proposed to play a role in the initiation of neuronal death, and apoptosis as revealed by TUNEL staining. Rat brains were investigated immunohistochemically 2 h to 21 days after exposure to impulse noise of 198 dB or 202 dB. c-Jun was expressed in neuronal perikarya in layers II-VI of the temporal cortex, the cingulate and the piriform cortices at 2 h to 21 days after both exposure levels. Granule neurons of the dentate gyrus and the CA1-3 in the hippocampus pyramidal neurons were similarly affected. The elevated expression of c-Jun products remained high at all postexposure times. TUNEL staining was positive among the same nerve cell populations 6 h after exposure and persisted even at 7 days at both exposure levels.