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Expression of c-Fos and c-Myc and deposition of beta-APP in neurons in the adult rat brain as a result of exposure to short-lasting impulse noise.

Artikel i vetenskaplig tidskrift
Författare Annette Säljö
Feng Bao
Jingshan Shi
Anders Hamberger
Hans-Arne Hansson
Kenneth Haglid
Publicerad i Journal of neurotrauma
Volym 19
Nummer/häfte 3
Sidor 379-85
ISSN 0897-7151
Publiceringsår 2002
Publicerad vid Institutionen för anatomi och cellbiologi
Sidor 379-85
Språk en
Länkar dx.doi.org/10.1089/0897715027535949...
Ämnesord Amyloid beta-Protein Precursor, biosynthesis, metabolism, Animals, Astrocytes, metabolism, Brain, metabolism, Brain Chemistry, physiology, Brain Injuries, etiology, metabolism, Cerebral Cortex, metabolism, Female, Hippocampus, metabolism, Immediate-Early Proteins, biosynthesis, metabolism, Immunohistochemistry, Models, Animal, Neurons, metabolism, Noise, adverse effects, Proto-Oncogene Proteins c-fos, biosynthesis, metabolism, Proto-Oncogene Proteins c-myb, biosynthesis, metabolism, Rats, Rats, Wistar
Ämneskategorier Neurovetenskap

Sammanfattning

There is increasing evidence that impulse noise causes brain damage, but little is known about the mechanisms and extent of the response. Here, rat brains were investigated immunohistochemically for the expression of c-Fos, c-Myc, and beta-APP during the first 3 weeks postexposure to impulse noise of 198 or 202 dB. The expression of c-Fos and c-Myc increased at 2 h after exposure in neurons of the cerebral cortex, thalamus, and hippocampus, and this c-Fos immunoreactivity remained elevated for the entire observation period. The c-Myc immunoreactivity peaked at 18 h in both neurons and astrocytes but returned to control levels at 7 days. Abnormal deposition of beta-APP was evident within 6 h in the same brain regions. The beta-APP immunoreactivity was most prominent at 18 h and remained increased over the 21-day period assessed. The observed effects were similar to those described in humans following traumatic brain injury and in Alzheimer's disease. We conclude that impulse noise influences the brain in a fashion similar to that in cases with progressive CNS degeneration.

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