Traumatic brain injury alters long-term hippocampal neuron morphology in juvenile, but not immature, rats
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Updated: Apr 28, 2026
Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury
Published on: November 19, 2012
Eric M Casella1, Theresa Currier Thomas, Dana L Vanino
1Barrow Neurological Institute, Phoenix Children's Hospital, Ambulatory Building B, 4th Floor, 1919 East Thomas Road, Phoenix, AZ, 85016, USA.
Insights
Pediatric traumatic brain injury (TBI) in juvenile rats at post-natal day 17 caused lasting hippocampal neuron changes. Injury at an earlier age (post-natal day 7) did not result in these structural alterations.
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Traumatic Brain Injury Research
Background:
- Pediatric traumatic brain injury (TBI) significantly impacts brain development.
- Neuropathological cascades in the juvenile brain can lead to cognitive deficits.
- Understanding age-dependent responses to TBI is crucial for predicting long-term outcomes.
Purpose of the Study:
- To investigate the long-term structural consequences of experimental TBI in juvenile rats.
- To determine if TBI-induced behavioral deficits correlate with quantifiable changes in hippocampal neurons.
- To assess the influence of age at injury on neuronal morphology post-TBI.
Main Methods:
- Controlled cortical impact (CCI) model used to induce TBI in juvenile rats at post-natal day (PND) 17 and PND7.
- Hippocampal neuronal morphology quantified using Golgi-Cox staining at post-injury day 28 (PID28).
- Analysis focused on dentate gyrus (DG), CA3, and CA1 regions, examining soma area, dendritic length, and branching.
Main Results:
- Significant increase in soma area of DG and CA3 neurons in PND17 rats at PID28 compared to controls.
- Significant decrease in dendritic length and branching in CA1 neurons of PND17 rats at PID28.
- No significant morphological changes observed in CA1 neurons of PND7 rats at PID28, suggesting age-dependent effects.
Conclusions:
- Long-lasting structural alterations in hippocampal neurons occur following TBI in PND17 juvenile rats.
- Immature PND7 rats exhibit differential plasticity and do not show similar morphological changes post-TBI.
- Age at the time of injury plays a critical role in the long-term structural response of the developing brain.
Purpose:
Pediatric traumatic brain injury (TBI) represents a prominent yet understudied medical condition that can profoundly impact brain development. As the juvenile injured brain matures in the wake of neuropathological cascades during potentially critical periods, circuit alterations may explain neurological consequences, including cognitive deficits. We hypothesize that experimental brain injury in juvenile rats, with behavioral deficits that resolve, will lead to quantifiable structural changes in hippocampal neurons at chronic time points post-injury.
Methods:
Controlled cortical impact (CCI), a model of focal TBI with contusion, was used to induce brain injury on post-natal day (PND) 17 juvenile rats. The histological consequence of TBI was quantified in regions of the hippocampus at post-injury day 28 (PID28) on sections stained using a variation of the Golgi-Cox staining method. Individual neuronal morphologies were digitized from the dentate gyrus (DG), CA3, and CA1 regions.
Results:
Soma area in the ipsilateral injured DG and CA3 regions of the hippocampus increased significantly at PID28 in comparison to controls. In CA1, dendritic length and dendritic branching decreased significantly in comparison to controls and the contralateral hemisphere, without change in soma area. To extend the study, we examined neuronal morphology in rats with CCI at PND7. On PID28 after CCI on PND7 rats, CA1 neurons showed no injury-induced change in morphology, potentially indicating an age-dependent morphological response to injury.
Conclusions:
Long-lasting structural alterations in hippocampal neurons of brain-injured PND17 juvenile animals, but not PND7 immature animals, suggest differential plasticity depending on age-at-injury, with potential consequences for later function.
