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Previous Article | Next Article
The Journal of Neuroscience, January 15, 2000, 20(2):763-770
Cyclooxygenase-2 Contributes to Functional Hyperemia in Whisker-Barrel Cortex
Kiyoshi Niwa1, Eiichi Araki1, Scott G. Morham2, M. Elizabeth Ross1, and Costantino Iadecola1 1 Center for Clinical and Molecular Neurobiology, Departments of Neurology and Neuroscience, University of Minnesota Medical School, Minneapolis, Minnesota 55455, and 2 Myriad Genetics, Salt Lake City, Utah 84108
The prostanoid-synthesizing enzyme cyclooxygenase-2 (COX-2) is expressed in selected cerebral cortical neurons and is involved in synaptic signaling. We sought to determine whether COX-2 participates in the increase in cerebral blood flow produced by synaptic activity in the somatosensory cortex. In anesthetized mice, the vibrissae were stimulated mechanically, and cerebral blood flow was recorded in the contralateral somatosensory cortex by a laser-Doppler probe. We found that the COX-2 inhibitor NS-398 attenuates the increase in somatosensory cortex blood flow produced by vibrissal stimulation. Furthermore, the flow response was impaired in mice lacking the COX-2 gene, whereas the associated increase in whisker-barrel cortex glucose use was not affected. The increases in cerebral blood flow produced by hypercapnia, acetylcholine, or bradykinin were not attenuated by NS-398, nor did they differ between wild-type and COX-2 null mice. The findings provide evidence for a previously unrecognized role of COX-2 in the mechanisms coupling synaptic activity to neocortical blood flow and provide an insight into one of the functions of constitutive COX-2 in the CNS.
Key words: cerebral blood flow; somatosensory activation; glucose use; prostanoids; 2-deoxyglucose; COX-2 knock-out mice; NS-398
Copyright © 2000 Society for Neuroscience 0270-6474/00/202763-08$05.00/0
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