Abstract
Recovery following Traumatic Brain Injury (TBI) can vary tremendously among individuals. Lifestyle following injury, including differential social interactions, may modulate the extent of secondary injury following TBI. To examine this possibility under controlled conditions, closed head injury (CHI) was induced in C57Bl6 mice using a standardized weight drop device after which mice were either housed in isolation or with their original cagemates (“socially-housed”) for 4 weeks. CHI transiently impaired novel object recognition (NOR) in both isolated and social mice, confirming physical and functional injury. By contrast, Y maze navigation was impaired in isolated but not social mice at 1–4 weeks post CHI. CHI increased excitotoxic signaling in hippocampal slices from all mice, which was transiently exacerbated by isolation at 2 weeks post CHI. CHI slightly increased reactive oxygen species and did not alter levels of amyloid beta (Abeta), total or phospho-tau, total or phosphorylated neurofilaments. CHI increased serum corticosterone in both groups, which was exacerbated by isolation. These findings support the hypothesis that socialization may attenuate secondary damage following TBI. In addition, a dominance hierarchy was noted among socially-housed mice, in which the most submissive mouse displayed indices of stress in the above analyses that were statistically identical to those observed for isolated mice. This latter finding underscores that the nature and extent of social interaction may need to vary among individuals to provide therapeutic benefit.
Highlights
Traumatic Brain Injury (TBI) affects over 2 million Americans each year, resulting in >$70 billion in direct and indirect expenditures since 2000
We utilized the reductionist approach of reproducible, experimental closed head injuries (CHI) in mice in efforts to determine whether or not social interaction could influence secondary injury
We considered that monitoring mice within 24 h after injury, followed by weekly observations for 1 month, would afford insight into whether any impact of CHI on cognitive or physiological parameters was derived exclusively from primary and/or secondary injury
Summary
Traumatic Brain Injury (TBI) affects over 2 million Americans each year, resulting in >$70 billion in direct and indirect expenditures since 2000. The majority (>75%) of instances of TBI are classified as closed head injuries (CHI; Corso et al, 2006; Finkelstein et al, 2006; Faul et al, 2010). Primary injury encompasses structural damage characterized by the stretching, compression, and tearing of blood vessels and tissue, the extent of which is dependent upon the nature of impact (Maas et al, 2008). Integrity of the white-matter tracts is compromised via shearing forces resulting in both axonal and myelin damage; the extent of this white-matter damage has been correlated with reduced cognitive function (Niogi et al, 2008).
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