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Updated: Feb 12, 2026

A Novel Model of Mild Traumatic Brain Injury for Juvenile Rats
Published on: December 8, 2014
BDNF expression increases without changes in play behavior following concussion in juvenile rats (Rattus Norvegicus)
Allison C F Dyck1, Tammy L Ivanco1,2
1a Department of Psychology , University of Manitoba, Winnipeg, Manitoba, Canada.
Insights
Mild traumatic brain injury (mTBI) in young children can cause lasting impairments. This study found increased brain-derived neurotrophic factor (BDNF) in motor cortices after concussion, suggesting cellular changes.
Area of Science:
- Neuroscience
- Pediatric Traumatology
Background:
- Young children are susceptible to concussion (mild traumatic brain injury, mTBI).
- While some children recover fully, others experience persistent cognitive and motor deficits.
- Understanding mTBI's cellular mechanisms is crucial for effective treatment and recovery protocols.
Purpose of the Study:
- To investigate molecular and behavioral changes in a rat model simulating childhood concussion.
- To examine brain-derived neurotrophic factor (BDNF) levels in response to mTBI.
- To assess potential compensatory mechanisms following pediatric concussion.
Main Methods:
- A rat model was used, with injury or sham procedures performed at an age analogous to early human childhood.
- Behavioral analysis focused on social play patterns.
- Brain tissue (motor cortex and medial prefrontal cortex) was analyzed for BDNF protein levels.
Main Results:
- No significant differences in social play behavior were observed between mTBI and sham groups.
- BDNF levels were significantly elevated in both the impacted (right) and contralateral (left) motor cortices of the mTBI group compared to the medial prefrontal cortex.
- Elevated BDNF was also noted in the medial prefrontal cortex of the mTBI group relative to the sham group.
Conclusions:
- Concussion triggers ongoing cellular plasticity in both the direct impact zone and connected brain regions.
- These findings suggest that the brain initiates compensatory responses at the cellular level after injury.
- This highlights the brain's capacity for adaptation following mTBI, even in early development.
Purpose:
Young children have a high risk of concussion or mild traumatic brain injury (mTBI). Children often appear healthy soon after mTBI, but some have pervasive cognitive and/or motor impairments. Understanding underlying mechanisms recruited after concussion may help for return to play protocols and mitigating what might be lifelong impairments.
Methods:
We investigated molecular and behavioral changes in a rat model of childhood concussion. Rats received an injury or sham procedure at an age approximately equivalent to the human period of early childhood. Social play was analyzed for behavioral differences. Tissue from the right motor cortex (impacted), left motor cortex, and medial prefrontal cortex were analyzed for brain derived neurotrophic factor (BDNF) protein.
Results:
Play behavior was not significantly different between conditions. BDNF levels were much higher in both the right and left motor cortices of the mTBI group compared to medial prefrontal cortex, which is relatively remote from the impact site, within the mTBI group and all tissue collected from the sham group.
Conclusions:
There is ongoing plastic change at the cellular level in both the impacted area and the well-connected contralateral area after a concussion, suggesting compensatory mechanisms after injury are still at play.
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