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Lateral Fluid Percussion: Model of Traumatic Brain Injury in Mice
Published on: August 22, 2011
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Altered Neuroinflammatory Transcriptomic Profile in the Hippocampal Dentate Gyrus Three Weeks After Lateral Fluid
Anthony J DeSana1, Yara Alfawares1, Roshni Khatri1
1Department of Neurosurgery, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
International Journal of Molecular Sciences
|September 27, 2025
Summary
Traumatic brain injury (TBI) affects memory by damaging the hippocampus. This study reveals ongoing neuroinflammation in the dentate gyrus three weeks post-TBI, involving microglia and astrocytes.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathology
Background:
- Traumatic brain injury (TBI) is a leading cause of global disability, frequently resulting in cognitive and memory impairments.
- The hippocampus, crucial for learning and memory, is highly susceptible to TBI.
- Dysfunction in the hippocampal dentate gyrus is a key factor in TBI-related cognitive deficits, yet its transcriptomic changes remain poorly understood.
Purpose of the Study:
- To investigate the transcriptomic alterations within the dentate gyrus at subacute-to-chronic timepoints following TBI.
- To identify specific cellular and molecular changes contributing to cognitive deficits after TBI.
Main Methods:
- Lateral fluid percussion injury was induced in male rats.
- Bulk RNA sequencing and single-nucleus RNA sequencing were performed on isolated dentate gyrus tissue.
- Analyses were conducted three weeks post-injury.
Main Results:
- Evidence of a persistent neuroinflammatory response was detected in the dentate gyrus.
- Increased expression of neuroinflammatory genes was observed.
- Specific microglia and astrocyte populations were implicated in the observed inflammatory pathways.
Conclusions:
- The dentate gyrus exhibits ongoing neuroinflammation weeks after TBI.
- Transcriptomic analysis highlights the involvement of specific glial cell populations in TBI-induced neuroinflammation.
- These findings provide insights into the molecular mechanisms underlying TBI-related cognitive dysfunction.

