Both protein kinase G dependent and independent mechanisms are involved in the modulation of glutamate release by nitric oxide in rat hippocampal nerve terminals

Detalhes bibliográficos
Autor(a) principal: Sequeira, Sónia M.
Data de Publicação: 1999
Outros Autores: Carvalho, Arsélio P., Carvalho, Caetana M.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
Texto Completo: http://hdl.handle.net/10316/5466
https://doi.org/10.1016/S0304-3940(98)01002-7
Resumo: We 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.
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spelling Both protein kinase G dependent and independent mechanisms are involved in the modulation of glutamate release by nitric oxide in rat hippocampal nerve terminalsHippocampal synaptosomesGlutamate releaseNO donorsNitric oxideWe 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.http://www.sciencedirect.com/science/article/B6T0G-3VV6CCC-8/1/2aa25f5d4327b44780c9b8f12b64f2e11999info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleaplication/PDFhttp://hdl.handle.net/10316/5466http://hdl.handle.net/10316/5466https://doi.org/10.1016/S0304-3940(98)01002-7engNeuroscience Letters. 261:1-2 (1999) 29-32Sequeira, Sónia M.Carvalho, Arsélio P.Carvalho, Caetana M.info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2020-11-06T16:59:48Zoai:estudogeral.uc.pt:10316/5466Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T20:55:31.414295Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse
dc.title.none.fl_str_mv Both protein kinase G dependent and independent mechanisms are involved in the modulation of glutamate release by nitric oxide in rat hippocampal nerve terminals
title Both protein kinase G dependent and independent mechanisms are involved in the modulation of glutamate release by nitric oxide in rat hippocampal nerve terminals
spellingShingle Both protein kinase G dependent and independent mechanisms are involved in the modulation of glutamate release by nitric oxide in rat hippocampal nerve terminals
Sequeira, Sónia M.
Hippocampal synaptosomes
Glutamate release
NO donors
Nitric oxide
title_short Both protein kinase G dependent and independent mechanisms are involved in the modulation of glutamate release by nitric oxide in rat hippocampal nerve terminals
title_full Both protein kinase G dependent and independent mechanisms are involved in the modulation of glutamate release by nitric oxide in rat hippocampal nerve terminals
title_fullStr Both protein kinase G dependent and independent mechanisms are involved in the modulation of glutamate release by nitric oxide in rat hippocampal nerve terminals
title_full_unstemmed Both protein kinase G dependent and independent mechanisms are involved in the modulation of glutamate release by nitric oxide in rat hippocampal nerve terminals
title_sort Both protein kinase G dependent and independent mechanisms are involved in the modulation of glutamate release by nitric oxide in rat hippocampal nerve terminals
author Sequeira, Sónia M.
author_facet Sequeira, Sónia M.
Carvalho, Arsélio P.
Carvalho, Caetana M.
author_role author
author2 Carvalho, Arsélio P.
Carvalho, Caetana M.
author2_role author
author
dc.contributor.author.fl_str_mv Sequeira, Sónia M.
Carvalho, Arsélio P.
Carvalho, Caetana M.
dc.subject.por.fl_str_mv Hippocampal synaptosomes
Glutamate release
NO donors
Nitric oxide
topic Hippocampal synaptosomes
Glutamate release
NO donors
Nitric oxide
description We 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.
publishDate 1999
dc.date.none.fl_str_mv 1999
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
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dc.identifier.uri.fl_str_mv http://hdl.handle.net/10316/5466
http://hdl.handle.net/10316/5466
https://doi.org/10.1016/S0304-3940(98)01002-7
url http://hdl.handle.net/10316/5466
https://doi.org/10.1016/S0304-3940(98)01002-7
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Neuroscience Letters. 261:1-2 (1999) 29-32
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
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dc.format.none.fl_str_mv aplication/PDF
dc.source.none.fl_str_mv reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
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