Nitric oxide modulates agonist-evoked Ca2+ release and influx responses in PC12-64 cells

European Journal of Pharmacology
E ClementiG Nisticò

Abstract

Nitric oxide (NO) is a signalling molecule involved in events crucial to neuronal cell function such as neurotransmitter release, gene transcription, and neurotoxicity. In these, as well as in many other neuronal processes, a key role may be played by the increases of the intracellular Ca2+ concentration ([Ca2+]i) occurring in response to activation of plasma membrane receptors coupled to phosphatidylinositol 4,5-bisphosphate hydrolysis. Such a [Ca2+]i increases are sustained by release of the cation from intracellular stores and stimulation of influx through specific Ca2+ channels. We have investigated the role of NO in modulating the two above Ca2+ processes occurring subsequently to muscarinic receptor activation in a selected clone (PC12-64) of PC12 cells, a neurosecretory/neuronal cell model. Analysis of [Ca2+]i variations in fura-2-loaded cells, exposed to different NO synthase inhibitors or NO donors, showed that Ca2+ release from intracellular stores was moderately inhibited and stimulated by these two groups of drugs, respectively, while Ca2+ influx through the channels directly coupled to muscarinic receptors was found to be insensitive to NO action. In contrast, Ca2+ influx activated by muscarinic receptor-induced st...Continue Reading

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Citations

May 28, 2011·Cellular and Molecular Neurobiology·Hanwook KimSung-Woo Cho
Sep 18, 2012·International Journal of Developmental Neuroscience : the Official Journal of the International Society for Developmental Neuroscience·Juan CenBian-Sheng Ji
Dec 24, 2009·Alcoholism, Clinical and Experimental Research·Tara S Bender, Abdel A Abdel-Rahman
Aug 13, 1999·The American Journal of Physiology·E L WatsonS M Ott

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