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Updated: Jul 15, 2026
Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
Diffuse alterations in synaptic protein expression following focal traumatic brain injury in the immature rat
G T Gobbel1, C Bonfield, E B Carson-Walter
1Department of Neurological Surgery, University of Pittsburgh, Suite B-400, UPMC Presbyterian, 200 Lothrop Street, Pittsburgh, PA 15213, USA.
Insights
Traumatic brain injury (TBI) in young rats causes a decrease in the synaptic protein synaptophysin, which may explain cognitive decline. Recovery of this protein parallels cognitive improvements after injury.
Area of Science:
- Neuroscience
- Pediatric Traumatology
- Synaptic Plasticity
Background:
- Mechanisms of cognitive decline after pediatric traumatic brain injury (TBI) are not well understood.
- Synaptic alterations may play a role in TBI-induced cognitive deficits.
- This study investigates the impact of TBI on synaptophysin expression in an immature animal model.
Purpose of the Study:
- To examine the role of synaptic alterations in cognitive decline following pediatric TBI.
- To define the impact of TBI on synaptophysin expression in immature rats.
Main Methods:
- Traumatic brain injury (TBI) induced in postnatal day 17 (PND17) rats via controlled cortical impact.
- Immunohistochemistry and immunoblotting used to assess NeuN and synaptophysin expression.
- Evaluations conducted at 1 day, 1 week, and 1 month post-injury.
Main Results:
- Significant decreases in neuronal marker NeuN and synaptic protein synaptophysin observed 1 day and 1 week post-TBI in hippocampus and neocortex.
- These decreases were also noted in contralateral brain regions, indicating diffuse alterations.
- Synaptophysin and NeuN levels recovered by 1 month post-injury.
Conclusions:
- Decreased synaptophysin expression following experimental TBI in PND17 rats correlates with cognitive deficits.
- Synaptophysin changes may contribute to cognitive decline after immature TBI.
- Immature TBI can cause diffuse, not just focal, alterations in protein expression, impacting cognitive function.
Introduction:
The mechanisms responsible for cognitive decline after traumatic brain injury (TBI) in pediatric patients are poorly understood. The present study examined the potential role of synaptic alterations in this process by using an animal model of immature head injury to define the impact of TBI on expression of the synaptic protein, synaptophysin.
Materials And Methods:
After craniotomy, TBI was induced in postnatal day 17 (PND17) rats using controlled cortical impact delivered to the left hemisphere. NeuN, a neuronal marker, and synaptophysin expression were examined 1 day, 1 week, and 1 month after injury by immunohistochemistry and immunoblotting.
Results:
There were significant decreases in both NeuN and synaptophysin after 1 day and 1 week but not 1 month after injury within the hippocampus and neocortex adjacent to the impact site compared to sham-injured controls. The decrease in synaptophysin and NeuN was also noted in the contralateral hippocampus by 1 day after injury and in the contralateral neocortex by 1 week, indicating that changes in protein expression were not solely localized to the injury site but occurred in more distant regions as well.
Discussion:
In conclusion, the decrease and recovery in synaptophysin parallel the cognitive changes that occur after experimental TBI in the PND17 rat, which suggests that changes in this protein may contribute to cognitive declines after injury. The results also suggest that, in spite of the focal nature of the impact, diffuse alterations in protein expression can occur after immature TBI and may contribute to the subsequent cognitive dysfunction.
