Expression of c-Fos and c-Myc and Deposition of β-APP in Neurons in the Adult Rat Brain as a Result of Exposure to Short-Lasting Impulse Noise
- 1 March 2002
- journal article
- Published by Mary Ann Liebert Inc in Journal of Neurotrauma
- Vol. 19 (3) , 379-385
- https://doi.org/10.1089/089771502753594945
Abstract
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.Keywords
This publication has 38 references indexed in Scilit:
- N-Myc Shares Cellular Functions with c-MycDNA and Cell Biology, 2000
- Caspases and mitochondria in c-Myc-induced apoptosis: identification of ATM as a new target of caspasesOncogene, 2000
- Airbag associated fatal head injury: case report and review of the literature on airbag injuriesEmergency Medicine Journal, 2000
- Experimental Brain Injury Induces Expression of Amyloid Precursor Protein, Which May Be Related to Neuronal Loss in the HippocampusJournal of Neurotrauma, 1998
- Neuronal expression of AP-1 proteins in excitotoxic-neurodegenerative disorders and following nerve fiber lesionsProgress in Neurobiology, 1995
- A New Model for Rapid Stretch-Induced Injury of Cells in Culture: Characterization of the Model Using AstrocytesJournal of Neurotrauma, 1995
- Amyloid β-protein precursor: new clues to the genesis of Alzheimer's diseaseCurrent Opinion in Neurobiology, 1994
- Degeneration in vitro of post-mitotic neurons overexpressing the Alzheimer amyloid protein precursorNature, 1992
- The amyloid protein precursor of Alzheimer's disease is a mediator of the effects of nerve growth factor on neurite outgrowthNeuron, 1992
- Overexpression of amyloid precursor protein alters its normal processing and is associated with neurotoxicityBiochemical and Biophysical Research Communications, 1992