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Neuropathology and neurobehavioral alterations in a rat model of traumatic brain injury to occupants of vehicles targeted by underbody blasts.
- Source :
-
Experimental neurology [Exp Neurol] 2017 Mar; Vol. 289, pp. 9-20. Date of Electronic Publication: 2016 Dec 05. - Publication Year :
- 2017
-
Abstract
- Many victims of blast-induced traumatic brain injury are occupants of military vehicles targeted by land mines. Recently improved vehicle designs protect these individuals against blast overpressure, leaving acceleration as the main force potentially responsible for brain injury. We recently developed a unique rat model of under-vehicle blast-induced hyperacceleration where exposure to acceleration as low as 50G force results in histopathological evidence of diffuse axonal injury and astrocyte activation, with no evidence of neuronal cell death. This study investigated the effects of much higher blast-induced accelerations (1200 to 2800G) on neuronal cell death, neuro-inflammation, behavioral deficits and mortality. Adult male rats were subjected to this range of accelerations, in the absence of exposure to blast overpressure, and evaluated over 28days for working memory (Y maze) and anxiety (elevated plus maze). In addition, brains obtained from rats at one and seven days post-injury were used for neuropathology and neurochemical assays. Sixty seven percent of rats died soon after being subjected to blasts resulting in 2800G acceleration. All rats exposed to 2400G acceleration survived and exhibited transient deficits in working memory and long-term anxiety like behaviors, while those exposed to 1200 acceleration G force only demonstrated increased anxiety. Behavioral deficits were associated with acute microglia/macrophage activation, increased hippocampal neuronal death, and reduced levels of tight junction- and synapse- associated proteins. Taken together, these results suggest that exposure of rats to high underbody blast-induced G forces results in neurologic injury accompanied by neuronal apoptosis, neuroinflammation and evidence for neurosynaptic alterations.<br /> (Copyright © 2016 Elsevier Inc. All rights reserved.)
- Subjects :
- Acceleration adverse effects
Animals
Antigens, Differentiation metabolism
Brain metabolism
Brain Injuries, Traumatic mortality
Caspase 3 metabolism
Cyclin D1 metabolism
Disease Models, Animal
Disks Large Homolog 4 Protein
HSP70 Heat-Shock Proteins metabolism
Intracellular Signaling Peptides and Proteins metabolism
Male
Maze Learning physiology
Membrane Proteins metabolism
Nitric Oxide Synthase Type II metabolism
Rats
Rats, Sprague-Dawley
Time Factors
Zonula Occludens-1 Protein metabolism
von Willebrand Factor metabolism
Blast Injuries complications
Brain pathology
Brain Injuries, Traumatic etiology
Brain Injuries, Traumatic pathology
Gene Expression Regulation physiology
Subjects
Details
- Language :
- English
- ISSN :
- 1090-2430
- Volume :
- 289
- Database :
- MEDLINE
- Journal :
- Experimental neurology
- Publication Type :
- Academic Journal
- Accession number :
- 27923561
- Full Text :
- https://doi.org/10.1016/j.expneurol.2016.12.001