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

Artikel i vetenskaplig tidskrift
Författare Annette Säljö
Feng Bao
Shi Jingshan
Anders Hamberger
Hans-Arne Hansson
Kenneth Haglid
Publicerad i Journal of neurotrauma
Volym 19
Nummer/häfte 8
Sidor 985-91
ISSN 0897-7151
Publiceringsår 2002
Publicerad vid Institutionen för anatomi och cellbiologi
Sidor 985-91
Språk en
Länkar dx.doi.org/10.1089/0897715023203171...
Ämnesord 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
Ämneskategorier Neurovetenskap

Sammanfattning

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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