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    J Neurosci Res. 2008 Dec;86(16):3605-12.

    Genetic disruption of cyclooxygenase-2 does not improve histological or behavioral outcome after traumatic brain injury in mice.

    Ahmad M, Rose ME, Vagni V, Griffith RP, Dixon CE, Kochanek PM, Hickey RW, Graham SH.

    Source

    Geriatric Research Educational and Clinical Center, VA Pittsburgh Healthcare System, Pittsburgh, PA 15206, USA.

    Abstract

    Increasing evidence suggests a role for cyclooxygenase-2 (COX-2) in traumatic brain injury (TBI). In the present study, the role of COX-2 in TBI was investigated using COX-2 gene-disrupted (COX-2 null) mice and wild-type (WT) controls that were subjected to the controlled cortical impact (CCI) model of TBI. There was increased expression of COX-2 in ipsilateral hippocampus in WT mice subjected to CCI. CCI resulted in a significant increase in prostaglandin E(2) concentrations in WT compared with COX-2 null hippocampi. There was a significant increase in TUNEL staining of CA1 neurons 24 hr after CCI in WT, but not in COX-2 null mice, compared with sham-operated controls, which is consistent with a protective role for COX-2 in the early phase of injury after TBI. However, there was no difference in lesion volume 21 days after CCI in COX-2 null and WT mice. COX-2 gene disruption did not alter Morris water maze performance. Taken together, these results suggest only a minor role for COX-2 activity in determining outcome after TBI in mouse.

    (c) 2008 Wiley-Liss, Inc.

    PMID:
    18711748
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC2737709
    Free PMC Article

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