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Although activation of the N-methyl-D-aspartate (NMDA) receptor is thought to contribute to altered cerebrovascular regulation after traumatic brain injury, the effects of such injury on the vascular response to NMDA itself has been less well appreciated. The newly described opioid nociceptin/orphanin FQ (NOC/oFQ) elicits pial artery dilation, at least in part, in a prostaglandin-dependent manner and is released into cerebrospinal fluid after fluid percussion brain injury (FPI). Generation of superoxide anion (O(2)(-)) occurs after FPI, and a byproduct of cyclooxygenase metabolism is the generation of O(2)(-). This study was designed to determine whether NOC/oFQ generates O(2)(-), which in turn could link NOC/oFQ release to impaired NMDA-induced pial artery dilation after FPI.

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Superoxide Generation Links Nociceptin/Orphanin FQ (NOC/oFQ) Release to Impaired <i>N</i> -Methyl- <scp>d</scp> -Aspartate Cerebrovasodilation After Brain Injury

Superoxide Generation Links Nociceptin/Orphanin FQ (NOC/oFQ) Release to Impaired N -Methyl- d -Aspartate Cerebrovasodilation After Brain Injury