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Role of the nitric oxide/cyclic GMP pathway and ascorbic acid in 3-morpholinosydnonimine (SIN-1)-induced increases in dopamine secretion from PC12 cells: a microdialysis in vitro study

Serra, Pier Andrea and Migheli, Rossana and Rocchitta, Gaia Giovanna Maria and Taras, Maria Grazia and Mura, Maria P. and Delogu, Maria Rosaria and Esposito, Giovanni and Desole, Maria Speranza and Miele, Egidio and Miele, Maddalena (2003) Role of the nitric oxide/cyclic GMP pathway and ascorbic acid in 3-morpholinosydnonimine (SIN-1)-induced increases in dopamine secretion from PC12 cells: a microdialysis in vitro study. Neuroscience Letters, Vol. 353 (1), p. 5-8. ISSN 0304-3940. Article.

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DOI: 10.1016/j.neulet.2003.07.022

Abstract

We showed previously, using in vitro microdialysis, that activation of the nitric oxide (NO)/cyclic GMP pathway was the underlying mechanism of exogenous NO-induced dopamine (DA) secretion from PC12 cells. In this study, infusion of the potential peroxynitrite generator 3-morpholinosydnonimine (SIN-1, 1.0 mM for 60 min) induced a long-lasting decrease in dialysate DA þ 3-methoxytyramine (3- MT) in dialysates from PC12 cell suspensions. Ascorbic acid (0.2 mM) co-infusion allowed SIN-1 to increase dialysate DA þ 3-MT. SIN- 1 þ ascorbic acid effects were abolished by Ca2+ omission. Infusion of high K+ (75 mM) induced a 2.5-fold increase in dialysate DA þ 3- MT. The increase was inhibited by SIN-1 co-infusion. Conversely, co-infusion of ascorbic acid (0.2 mM) with SIN-1 þ high K+ resulted in a 3.5 fold increase in dialysate DA þ 3-MT. The L-type Ca2+ channel inhibitor nifedipine selectively inhibited the DA þ 3-MT increase pertaining to high K+, while the soluble guanylate cyclase (sGC) inhibitor 1H-[1,2,4]-oxadiazolo[4,3]quinoxalin-1-one selectively inhibited the increase pertaining to SIN-1 effects. These results suggest that activation of the NO/sGC/cyclic GMP pathway is the underlying mechanism of extracellular Ca2+-dependent effects of SIN-1 on DA secretion from PC12 cells. Extracellular Ca2+ entry occurs through nifedipine-insensitive channels. Ascorbic acid is a key determinant in modulating the distinct profiles of SIN-1 effects.

Item Type:Article
ID Code:5337
Status:Published
Refereed:Yes
Subjects:Area 05 - Scienze biologiche > BIO/14 Farmacologia
Divisions:001 Università di Sassari > 01 Dipartimenti > Neuroscienze, scienze materno infantili
Publisher:Elsevier Science Ireland
ISSN:0304-3940
Additional Information:PC12 cell, nitric oxide, cyclic GMP, calcium–dopamine secretion
Deposited On:21 Jan 2011 17:11

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