Abstract

The common carotid artery (CCA) supplies intra- and extra-cranial vascular beds. An area in the medulla controlling CCA blood flow is defined as the dorsal facial area (DFA) by Kuo et al. in 1987. In the DFA, presynaptic nitrergic and/or glutamatergic fibers innervate preganglionic nitrergic and/or cholinergic neurons which give rise to the preganglionic fibers of the parasympathetic 7th and 9th cranial nerves. Released glutamate from presynaptic nitrergic and/or glutamatergic fibers can activate N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors on preganglionic nitrergic and/or cholinergic neurons. By modulating this glutamate release, several neurochemicals including serotonin, arginine, nitric oxide, nicotine, choline and ATP in the DFA regulate CCA blood flow. Understanding the neurochemical regulatory mechanisms can provide important insights of the physiological roles of the DFA, and may help develop therapeutic strategies for diseases involving CCA blood flow, such as migraine, hypertensive disease, Alzheimer's disease and cerebral ischemic stroke.

Highlights

  • Common carotid artery (CCA) is an important artery supplying both intra- and extra-cranial tissues of the head, but the brain regulation of CCA blood flow has been rarely addressed

  • Pretreatment with either non-competitive NMDA receptor antagonist or amino-3-hydroxy-5-methylisoxazole-4propionic acid (AMPA)/ kainate receptor antagonist attenuates the glutamate-induced increase in CCA blood flow in a dose-dependent manner [13]. These findings demonstrate that NMDA and AMPA receptors on neurons in the dorsal facial area (DFA) are responsible for the increase in CCA blood flow

  • 5-HT reactive nerves are present in the DFA; they release 5-HT in tonic, which activates 5-HT2 receptors on the presynaptic nitrergic and/or glutamatergic fibers to cause an inhibition of glutamate release in the DFA, leading to the reduction in CCA blood flow

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Summary

Introduction

Common carotid artery (CCA) is an important artery supplying both intra- and extra-cranial tissues of the head, but the brain regulation of CCA blood flow has been rarely addressed. Neuronal release of glutamate is Carotid Flow Regulation by Medulla further confirmed by the findings that CCA blood flow increase induced by intra-DFA administrations of several neurochemicals, such as arginine (NO precursor), S-nitrosoN-acetylpenicillamine (NO donor) [18], ATP (P2 receptor agonist) [19], and choline (7-nAChR agonist) or nicotine (non-specific nAChR agonist), can be inhibited by glutamatergic receptor antagonists.

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