Cited by 157Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchAutomotive and Human Injury Biomechanics

Adaptation of the fluid percussion injury model to the mouse

CARBONELL, W. SHAWN, MARIS, DONALD O., McCALL, TODD, GRADY, M. SEAN·1998·Journal of Neurotrauma

Abstract

Fluid percussion injury (FPI) is a well-characterized experimental model of traumatic brain injury (TBI) in the rat. Many pathophysiologic consequences and mechanisms of recovery after TBI rely on neurochemical pathways that can be examined in genetically altered mice. Therefore, FPI applied to mice may be a useful experimental tool to investigate TBI at the molecular level. In the present study, we establish FPI as a viable model of TBI in the mouse by characterizing acute neurological, histopathological, and behavioral changes. Right-sided parasagittal FPI or sham treatment was administered in male C57BL/6 mice. Acute neurological evaluation revealed righting reflexes in the injured animals (p < 0.001). Deficits in spatial learning and memory were observed in the Morris water maze (MWM) 5 and 6 days after injury. A novel MWM data analysis protocol is described. The injured group (n = 18) demonstrated impaired performance in the MWM during acquisition (p < 0.05) and probe trials (p < 0.025) compared to sham animals (n = 16). At 7 days postinjury, glial fibrillary acidic protein immunohistochemistry revealed intense cortical, callosal, and hippocampal gliosis. The modified Gallyas silver degeneration stain consistently labeled cell bodies and terminals throughout the ipsilateral cortex, axons in the gray matter-white matter interface above the corpus callosum and within the corpus callosum bilaterally, and terminals and fibers in the thalamus bilaterally. Additionally, the mo…

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Crossref · 10.1089/neu.1998.15.217

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  • Many biological pathways are disrupted by experimental TBI resulting in progressive neurodegeneration including atrophy, neuronal loss, and axonal degeneration which are often associated with neuroinflammation including macrophage reactivity.

    “Many biological pathways are disrupted by experimental TBI resulting in progressive neurodegeneration including atrophy, neuronal loss, and axonal degeneration which are often associated with neuroinflammation including macrophage reactivity (82–85).”

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Authors
CARBONELL, W. S., MARIS, D. O., McCALL, T., & GRADY, M. S.
Affiliations
University of Washington (US)
Venue
Journal of Neurotrauma
Published
1998-03
Volume
15
Issue
3
Pages
217-229
ISSN
  • 0897-7151 (ISSN-L)
  • 1557-9042
OpenAlex
W1978835755
Cited by
157
References
0
Citations by year
2026: 2 · 2025: 6 · 2024: 6 · 2023: 4 · 2022: 2 · 2021: 6 · 2020: 7 · 2019: 10 · 2018: 10 · 2017: 10 · 2016: 13 · 2015: 5 · 2014: 9 · 2013: 11 · 2012: 4
FWCI
1.89
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurotrauma (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • University of Washington
  • National Institutes of Health (5p50ns030305-05, 5r01ns033107-03)
  • National Institute of Neurological Disorders and Stroke (NS-30305, NS33107)
Topics
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Automotive and Human Injury Biomechanics
Keywords
fluid percussion injury, traumatic brain injury, mouse model, spatial learning and memory, Morris water maze, gliosis, glial fibrillary acidic protein, corpus callosum, thalamus, righting reflex, behavioral deficits
MeSH terms
Animals, Brain Injuries, Postural Balance, Glial Fibrillary Acidic Protein, Gliosis, Male, Mice, Inbred C57BL, Neuroglia, Neurons, Silver Staining, Maze Learning, Mice, Rats

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