• Muzamil Ahmad, Marie E Rose, Vincent Vagni, Raymond P Griffith, C Edward Dixon, Patrick M Kochanek, Robert W Hickey, and Steven H Graham.
• Geriatric Research Educational and Clinical Center, VA Pittsburgh Healthcare System, Pittsburgh, PA 15206, USA.
• J. Neurosci. Res. 2008 Dec 1; 86 (16): 3605-12.

AbstractIncreasing 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.

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