Rocchitta, Gaia Giovanna Maria and Migheli, Rossana and Mura, Maria Pina and Esposito, Giovanni and Desole, Maria Speranza and Miele, Egidio and Miele, Maddalena and Serra, Pier Andrea (2004) Signalling pathways in the nitric oxide donor-induced dopamine release in the striatum of freely moving rats: evidence that exogenous nitric oxide promotes Ca2+ entry through store-operated channels. Brain Research, Vol. 1023 (2), p. 243-252. ISSN 0006-8993. Article.
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We showed previously, using in vitro microdialysis, that the activation of the soluble guanylate cyclase (sGC)/cyclic GMP pathway was the underlying mechanism of the extracellular Ca2+-dependent effects of exogenous NO on dopamine (DA) secretion from PC12 cells. In this study, the co-infusion of the sGC inhibitor 1H-[1,2,4]oxadiazolo[4,3] quinoxalin-1-one (ODQ) failed to affect the NO donor 3- morpholinosydnonimine (SIN-1, 5.0 mM)-induced DA increase (sevenfold baseline) in dialysates from the striatum of freely moving rats. Ca2+ omission from the perfusion fluid abolished baseline DA release but did not affect SIN-1-induced DA increases. The reintroduction of Ca2+ in the perfusion fluid restored the baseline dialysate DA; however, when Ca2+ reintroduction was associated with the infusion of either SIN-1 or the NO-donor S-nitrosoglutathione (SNOG), a sustained DA overflow was observed. DA overflow was selectively inhibited by the co-infusion of the store-operated channel blocker 2-aminoethoxydiphenyl borate. The chelation of intracellular Ca2+ by co-infusing 1,2-bis (o-amino-phenoxy)ethane-N,N,N’,N’-tetraacetic acid tetra (acetoxymethyl) ester (BAPTA-AM, 0.2 mM) greatly potentiated both SIN-1- and SNOG-induced increases in dialysate DA. BAPTA-AM-induced potentiation was inhibited by Ca2+ omission. We conclude that the sGC/ cyclic GMP pathway is not involved in the extracellular Ca2+-independent exogenous NO-induced striatal DA release; however, when intracellular Ca2+ is either depleted (by Ca2+ omission) or chelated (by BAPTA-AM co-infusion), exogenous NO does promote Ca2+ entry, most likely through store-operated channels, with a consequent further increase in DA release.
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