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標題: Nicotine stimulation of the medulla increases blood flow of the common carotid artery in cats
作者: Kuo, J.S.
Leung, Y.M.
Lin, N.N.
Lee, T.J.F.
Gong, C.L.
關鍵字: Carotid artery;Parasympathetic;Nicotinic acetylcholine receptor;Vascular control;dorsal facial area;nucleus-tractus-solitarius;in-vivo microdialysis;glutamate release;acetylcholine-receptors;synaptic-transmission;prefrontal cortex;neurons;rat;acid
Project: Autonomic Neuroscience-Basic & Clinical
期刊/報告no:: Autonomic Neuroscience-Basic & Clinical, Volume 152, Issue 1-2, Page(s) 49-54.
Microinjection of nicotine or glutamate into the dorsal facial area (DFA) of the medulla increases blood flow of common carotid artery (CCA). Whether there is a causal relationship between these two events is not known. Various agonists and antagonists for the nicotinic and glutamatergic receptors were microinjected through a four-barrel tubing into the DFA of anesthetized cats. Microinjections of nicotine [a non-selective nicotinic acetylcholine receptor (nAChR) agonist], choline (a selective alpha 7-nAChR agonist), glutamate or KCl induced a modest increase in CCA blood flow. The nicotine- and choline-induced increases were reduced by alpha-bungarotoxin (an alpha 7-nAChR antagonist) as well as MK-801 (a non-competitive NMDA receptor antagonist) or glutamate diethylester (a competitive AMPA/kainate receptor antagonist). The glutamate or KCl-induced increases were blocked by MK-801 and glutamate diethylester, but not by alpha-bungarotoxin. In conclusion, activation of nAChRs primarily via alpha 7-nAChR caused a release of glutamate, which in turn activated NMDA and AMPA receptors, while cholinergic substance was not released into the DFA to activate the nicotinic receptor. Crown Copyright (C) 2009 Published by Elsevier B.V. All rights reserved.
ISSN: 1566-0702
DOI: 10.1016/j.autneu.2009.08.019
Appears in Collections:期刊論文

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