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Updated: Feb 10, 2026
A Mouse Model of Single and Repetitive Mild Traumatic Brain Injury
Published on: June 20, 2017
Metabolic and Structural Imaging at 7 Tesla After Repetitive Mild Traumatic Brain Injury in Immature Rats
Emin Fidan1, Lesley M Foley2,3, Lee Ann New1
11 Safar Center for Resuscitation Research, Department of Critical Care Medicine, University of Pittsburgh, PA, USA.
Insights
Mild traumatic brain injury (mTBI) and repeated mild traumatic brain injury (rmTBI) in young rats cause significant white matter and neurochemical changes. Advanced imaging detected these subtle alterations, offering insights into potential disability and therapeutic targets in immature brains.
Area of Science:
- Neuroscience
- Radiology
- Pediatric Traumatology
Background:
- Mild traumatic brain injury (mTBI) is a common pediatric issue, often with normal initial imaging, increasing risk for repeated injury (rmTBI).
- Sensitive imaging techniques are needed to detect subtle neurophysiological changes after mTBI and rmTBI in immature brains.
Purpose of the Study:
- To investigate neurochemical and white matter alterations in immature rat brains following single and repeated mild traumatic brain injuries (mTBI and rmTBI).
- To assess the utility of advanced imaging techniques, including diffusion tensor imaging (DTI) and proton magnetic resonance spectroscopy (1H-MRS), in detecting injury-related changes.
Main Methods:
- Utilized 7 Tesla 1H-MRS and DTI on 18-day-old male rats at 7 days post-injury (single mTBI, rmTBI, or sham).
- Assessed traumatic axonal injury via beta-amyloid precursor protein (β-APP) immunohistochemistry.
- Analyzed changes in fractional anisotropy (FA), axial diffusivity (AD), radial diffusivity (RD), and metabolite ratios (NAA/Cr, Ins/Cr, Cho/Cr, Lip/Cr).
Main Results:
- DTI revealed decreased FA and increased AD/RD in white matter regions after mTBI, more pronounced after rmTBI.
- β-APP accumulation was observed in the external capsule post-mTBI and rmTBI.
- 1H-MRS showed reduced N-acetylaspartate/creatine (NAA/Cr) and increased myoinositol/creatine (Ins/Cr) ratios post-injury.
- rmTBI exacerbated NAA/Cr reduction and decreased choline/creatine (Cho/Cr) and lipid/creatine (Lip/Cr) ratios compared to sham and mTBI.
Conclusions:
- DTI and 1H-MRS can detect subtle white matter and neurochemical alterations in immature brains after mTBI and rmTBI.
- Observed changes in NAA, Ins, Cho, and Lip suggest neuro-axonal damage and glial responses.
- Findings highlight the potential for advanced imaging to inform understanding of disability and identify therapeutic targets for pediatric brain injury.
Abstract:
Mild traumatic brain injury (mTBI) in children is a common and serious public health problem. Traditional neuroimaging findings in children who sustain mTBI are often normal, putting them at risk for repeated mTBI (rmTBI). There is a need for more sensitive imaging techniques capable of detecting subtle neurophysiological alterations after injury. We examined neurochemical and white matter changes using diffusion tensor imaging of the whole brain and proton magnetic resonance spectroscopy of the hippocampi at 7 Tesla in 18-day-old male rats at 7 days after mTBI and rmTBI. Traumatic axonal injury was assessed by beta-amyloid precursor protein accumulation using immunohistochemistry. A significant decrease in fractional anisotropy and increase in axial and radial diffusivity were observed in several brain regions, especially in white matter regions, after a single mTBI versus sham and more prominently after rmTBI. In addition, we observed accumulation of beta-amyloid precursor protein in the external capsule after mTBI and rmTBI. mTBI and rmTBI reduced the N-acetylaspartate/creatine ratio (NAA/Cr) and increased the myoinositol/creatine ratio (Ins/Cr) versus sham. rmTBI exacerbated the reduction in NAA/Cr versus mTBI. The choline/creatine (Cho/Cr) and (lipid/Macro Molecule 1)/creatine (Lip/Cr) ratios were also decreased after rmTBI versus sham. Diffusion tensor imaging findings along with the decrease in Cho and Lip after rmTBI may reflect damage to axonal membrane. NAA and Ins are altered at 7 days after mTBI and rmTBI likely reflecting neuro-axonal damage and glial response, respectively. These findings may be relevant to understanding the extent of disability following mTBI and rmTBI in the immature brain and may identify possible therapeutic targets.
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