Traumatic brain injury in mice deficient in poly-ADP(ribose) polymerase: a preliminary report.

M. J. Whalen, R. S. Clark, C. E. Dixon, P. Robichaud, D. W. Marion, V. Vagni, S. Graham, L. Virag, G. Hasko, R. Stachlewitz, C. Szabo, P. M. Kochanek

    Research output: Contribution to journalArticle

    18 Scopus citations

    Abstract

    Poly (ADP-ribose) polymerase (PARP) is a ubiquitous nuclear enzyme that, when activated by free-radical induced DNA damage, contributes to energy failure and cell death in models of central nervous system ischemia and reperfusion. PARP contributes to neuronal cell death in vivo after cerebral ischemia/reperfusion, however, the role of PARP in the pathogenesis of traumatic brain injury (TBI) is unknown. We hypothesized that, compared to wild type mice (+/+), mice deficient in PARP (-/-) would have reduced motor and cognitive deficits after TBI. Mice underwent controlled cortical impact (CCI) (6 m/s, 1.2 mm depth) and were tested for motor (d 1-5) and cognitive (d 14-18) function after CCI. PARP -/- mice demonstrated improved motor performance and improved cognitive function after CCI (both p < 0.05 compared to +/+). This is the first study to evaluate a role for PARP in functional outcome after TBI. The results suggest a detrimental role for PARP in the pathogenesis of TBI.

    Original languageEnglish (US)
    Pages (from-to)61-64
    Number of pages4
    JournalActa neurochirurgica. Supplement
    Volume76
    StatePublished - 2000

    ASJC Scopus subject areas

    • Surgery
    • Clinical Neurology

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    Whalen, M. J., Clark, R. S., Dixon, C. E., Robichaud, P., Marion, D. W., Vagni, V., Graham, S., Virag, L., Hasko, G., Stachlewitz, R., Szabo, C., & Kochanek, P. M. (2000). Traumatic brain injury in mice deficient in poly-ADP(ribose) polymerase: a preliminary report. Acta neurochirurgica. Supplement, 76, 61-64.