Interaction of mechanisms involving epoxyeicosatrienoic acids, adenosine receptors, and metabotropic glutamate receptors in neurovascular coupling in rat whisker barrel cortex.
Interaction of mechanisms involving epoxyeicosatrienoic acids, adenosine receptors, and metabotropic glutamate receptors in neurovascular coupling in rat whisker barrel cortex.
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大鼠须桶皮层神经血管耦合中涉及环氧二十碳三烯酸、腺苷受体和代谢型谷氨酸受体的机制的相互作用。
DOI：
10.1038/sj.jcbfm.9600511
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发表时间：
2008
期刊：
影响因子：
--
通讯作者：
Koehler,RaymondC
中科院分区：
文献类型：
--
作者：
Shi,Yanrong;Liu,Xiaoguang;Gebremedhin,Debebe;Falck,JohnR;Harder,DavidR;Koehler,RaymondC
Adenosine, astrocyte metabotropic glutamate receptors (mGluRs), and epoxyeicosatrienoic acids (EETs) have been implicated in neurovascular coupling. Although A2Aand A2Breceptors mediate cerebral vasodilation to adenosine, the role of each receptor in the cerebral blood flow (CBF) response to neural activation remains to be fully elucidated. In addition, adenosine can amplify astrocyte calcium, which may increase arachidonic acid metabolites such as EETs. The interaction of these pathways was investigated by determining if combined treatment with antagonists exerted an additive inhibitory effect on the CBF response. During whisker stimulation of anesthetized rats, the increase in cortical CBF was reduced by approximately half after individual administration of A2B, mGluR and EET antagonists and EET synthesis inhibitors. Combining treatment of either a mGluR antagonist, an EET antagonist, or an EET synthesis inhibitor with an A2Breceptor antagonist did not produce an additional decrement in the CBF response. Likewise, the CBF response also remained reduced by ∼50% when an EET antagonist was combined with an mGluR antagonist or an mGluR antagonist plus an A2Breceptor antagonist. In contrast, A2Aand A3receptor antagonists had no effect on the CBF response to whisker stimulation. We conclude that (1) adenosine A2Breceptors, rather than A2Aor A3receptors, play a significant role in coupling cortical CBF to neuronal activity, and (2) the adenosine A2Breceptor, mGluR, and EETs signaling pathways are not functionally additive, consistent with the possibility of astrocytic mGluR and adenosine A2Breceptor linkage to the synthesis and release of vasodilatory EETs.
