Journal
EXPERIMENTAL BRAIN RESEARCH
Volume 205, Issue 1, Pages 103-114Publisher
SPRINGER
DOI: 10.1007/s00221-010-2342-z
Keywords
Traumatic brain injury; Inflammation; Complement; Neurodegeneration; Strain dependent; T cells; Polymorphonuclear cells
Categories
Funding
- European Union
- NeuroproMiSe [LSHM-CT-2005-018637]
- EURATools [LSHG-CT-2005-019015]
- Wadsworth Foundation
- Torsten and Ragnar Soderberg's Foundation
- Bjorklund's Foundation
- Nils and Bibbi Jenssen's Foundation
- Montel Williams Foundation, Magn
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Secondary brain damage following traumatic brain injury in part depends on neuroinflammation, a process where genetic factors may play an important role. We examined the response to a standardized cortical contusion in two different inbred rat strains, Dark Agouti (DA) and Piebald Virol Glaxo (PVG). Both are well characterized in models of autoimmune neuroinflammation, where DA is susceptible and PVG resistant. We found that infiltration of polymorphonuclear granulocytes (PMN) at 3-day postinjury was more pronounced in PVG. DA was more infiltrated by T cells at 3-day postinjury, showed an enhanced glial activation at 7-day postinjury and higher expression of C3 complement at 7-day postinjury. Neurodegeneration, assessed by Fluoro-Jade, was also more pronounced in the DA strain at 30-day postinjury. These results demonstrate differences in the response to cortical contusion injury attributable to genetic influences and suggest a link between injury-induced inflammation and neurodegeneration. Genetic factors that regulate inflammation elicited by brain trauma may be important for the development of secondary brain damage.
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