Cyclooxygenase-2 contributes to functional hyperemia in whisker-barrel cortex
Cyclooxygenase-2 contributes to functional hyperemia in whisker-barrel cortex
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DOI：
10.1523/jneurosci.20-02-00763.2000
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发表时间：
2000-01-15
影响因子：
5.3
通讯作者：
Iadecola, C
中科院分区：
文献类型：
--
作者：
Niwa, K;Araki, E;Iadecola, C
前列腺素合成酶环氧合酶-2(COX-2)在选定的大脑皮层神经元中表达，并参与突触信号转导。我们试图确定COX-2是否参与了躯体感觉皮层突触活动所产生的脑血流量的增加。在麻醉小鼠中，机械刺激触须，并用激光多普勒探头记录对侧躯体感觉皮质的脑血流量。我们发现，COX-2抑制剂NS-398可以减弱由振动刺激引起的体感皮质血流量的增加。此外，缺乏COX-2基因的小鼠的血流反应受到损害，而相关的胡须桶皮质葡萄糖使用量的增加并未受到影响。NS-398不能减弱高碳酸血症、乙酰胆碱或缓激肽引起的脑血流量增加，野生型和COX-2基因缺失的小鼠之间也没有区别。这些发现为COX-2在突触活动与新皮质血流耦合机制中先前未知的作用提供了证据，并为深入了解COX-2在中枢神经系统中的构成功能之一提供了证据。
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.