Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/5466
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dc.contributor.authorSequeira, Sónia M.-
dc.contributor.authorCarvalho, Arsélio P.-
dc.contributor.authorCarvalho, Caetana M.-
dc.date.accessioned2008-09-01T15:42:46Z-
dc.date.available2008-09-01T15:42:46Z-
dc.date.issued1999en_US
dc.identifier.citationNeuroscience Letters. 261:1-2 (1999) 29-32en_US
dc.identifier.urihttp://hdl.handle.net/10316/5466-
dc.description.abstractWe compared the effects of sodium nitroprusside (SNP), and of 8-bromo guanosine 3',5'-cyclic monophosphate (8-BrcGMP), on the 4-aminopyridine (4-AP)-evoked Ca2+-dependent release of glutamate from hippocampal nerve terminals and further investigated the role of protein kinase G (PKG) in this mechanism. SNP and 8-BrcGMP dose-dependently inhibited glutamate release, however SNP concentrations ([SNP])>500 [mu]M abolished the 4-AP evoked release, whereas 8-BrcGMP maximally inhibited the release by about 30%. The inhibition of glutamate release at low concentrations of SNP (<=5 [mu]M) was of about 20%, and was reversed by Rp-8(4-chlorophenylthio)guanosine-3',5'-cyclic-monophosphorotioate) (RpCPTcGMP, 50 nM), but the inhibition at higher concentrations (5<SNP<=50 [mu]M) was insensitive to the PKG inhibitor, but sensitive to [1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one] (ODQ), which partially prevented the inhibition. [SNP]>50 [mu]M strongly inhibited glutamate release, and this was not reversed by either inhibitor. Furthermore, [SNP]<=50 [mu]M enhanced cGMP formation, and the observed effects were not related to either decreased Ca2+ entry or ATP/ADP levels. Our results indicate that NO/PKG is the signaling pathway underlying the inhibition of glutamate release at low concentrations of NO, and imply that other NO-dependent, but PKG-independent, mechanisms are activated and have complementary roles at higher NO concentrations.en_US
dc.description.urihttp://www.sciencedirect.com/science/article/B6T0G-3VV6CCC-8/1/2aa25f5d4327b44780c9b8f12b64f2e1en_US
dc.format.mimetypeaplication/PDFen
dc.language.isoengeng
dc.rightsopenAccesseng
dc.subjectHippocampal synaptosomesen_US
dc.subjectGlutamate releaseen_US
dc.subjectNO donorsen_US
dc.subjectNitric oxideen_US
dc.titleBoth protein kinase G dependent and independent mechanisms are involved in the modulation of glutamate release by nitric oxide in rat hippocampal nerve terminalsen_US
dc.typearticleen_US
dc.identifier.doi10.1016/S0304-3940(98)01002-7-
item.grantfulltextopen-
item.fulltextCom Texto completo-
item.languageiso639-1en-
Appears in Collections:FCTUC Ciências da Vida - Artigos em Revistas Internacionais
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