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Exposure to short-lasting impulse noise causes neuronal c-Jun expression and induction of apoptosis in the adult rat brain.

Journal article
Authors Annette Säljö
Feng Bao
Shi Jingshan
Anders Hamberger
Hans-Arne Hansson
Kenneth Haglid
Published in Journal of neurotrauma
Volume 19
Issue 8
Pages 985-91
ISSN 0897-7151
Publication year 2002
Published at Institute of Anatomy and Cell Biology
Pages 985-91
Language en
Keywords Animals, Apoptosis, physiology, Brain Injuries, etiology, metabolism, Cerebral Cortex, metabolism, physiopathology, Female, Head Injuries, Closed, etiology, metabolism, Immunohistochemistry, In Situ Nick-End Labeling, Noise, adverse effects, Proto-Oncogene Proteins c-jun, biosynthesis, Rats, Rats, Wistar
Subject categories Neuroscience


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.

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