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Low-intensity Blast Wave Model for Preclinical Assessment of Closed-head Mild Traumatic Brain Injury in Rodents
Published on: November 6, 2020
Low level primary blast injury in rodent brain
Pamela B L Pun1, Enci Mary Kan, Agus Salim
1Combat Care Laboratory, Defence Medical and Environmental Research Institute, DSO National Laboratories Singapore.
Frontiers in Neurology
|May 5, 2011
Summary
Mild traumatic brain injuries from blast waves show cellular damage and altered gene expression in rodents, with signs of recovery over time. Further research is needed to understand long-term effects.
Area of Science:
- Neuroscience
- Trauma Research
- Molecular Biology
Background:
- Blast attacks are increasing, leading to a rise in traumatic brain injuries.
- Primary blast waves are a significant mechanism for causing brain injury.
Purpose of the Study:
- To investigate the effects of single sub-lethal blast over pressure (BOP) on rodent brains.
- To analyze cellular and genetic changes following blast exposure.
Main Methods:
- Rodents were exposed to BOP levels of 48.9 kPa or 77.3 kPa.
- Brain tissue underwent microarray and histopathological analyses.
- TUNEL and caspase-3 staining identified DNA damage and apoptosis; APP staining indicated axonal damage.
Main Results:
- Cortical neurons showed shrinkage and vascular narrowing, with recovery by day 7.
- DNA-damaged oligodendrocytes and astrocytes were found in white matter, with minimal apoptosis.
- Over 5786 genes were altered, with 10 key genes suggesting repair mechanisms by days 4 and 7.
Conclusions:
- Sub-lethal BOP exposure causes mild, transient brain injury, affecting neurons, vasculature, and white matter.
- Observed cellular and genetic changes indicate a resolution process.
- Further investigation is required to determine if these changes normalize completely.
