Synaptic vesicle Ca2+/H+ antiport: dependence on the proton electrochemical gradient
Autor(a) principal: | |
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Data de Publicação: | 1999 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | http://hdl.handle.net/10316/5462 https://doi.org/10.1016/S0169-328X(99)00183-7 |
Resumo: | Synaptic vesicles isolated from sheep brain cortex accumulate Ca2+ by a mechanism of secondary active transport associated to the H+-pump activity. The process can be visualized either by measuring Ca2+-induced H+ release or [Delta]pH-dependent Ca2+ accumulation. We observed that the amount of Ca2+ taken up by the vesicles increases with the magnitude of the [Delta]pH across the membrane, particularly at Ca2+ concentrations (~500 [mu]M) found optimal for the antiporter activity. Similarly, H+ release induced by Ca2+ increased with the magnitude of [Delta]pH. However, above 60% [Delta]pH (high H+-pump activity), the net H+ release from the vesicles decreased as the pump-mediated H+ influx exceeded the Ca2+-induced H+ efflux. We also observed that the Ca2+/H+ antiport activity depends, essentially, on the [Delta]pH component of the electrochemical gradient (~3 nmol Ca2+ taken up/mg protein), although the [Delta][phi] component may also support some Ca2+ accumulation by the vesicles (~1 nmol/mg protein) in the absence of [Delta]pH. Both Ca2+-induced H+ release and [Delta]pH-dependent Ca2+ uptake could be driven by an artificially imposed proton motive force. Under normal conditions (H+ pump-induced [Delta]pH), the electrochemical gradient dependence of Ca2+ uptake by the vesicles was checked by inhibition of the process with specific inhibitors (bafilomycin A1, ergocryptin, folymicin, DCCD) of the H+-pump activity. These results indicate that synaptic vesicles Ca2+/H+ antiport is indirectly linked to ATP hydrolysis and it is essentially dependent on the chemical component ([Delta]pH) of the electrochemical gradient generated by the H+-pump activity. |
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Synaptic vesicle Ca2+/H+ antiport: dependence on the proton electrochemical gradientCa2+/H+ antiportSynaptic vesicleBrain cortexSynaptic vesicles isolated from sheep brain cortex accumulate Ca2+ by a mechanism of secondary active transport associated to the H+-pump activity. The process can be visualized either by measuring Ca2+-induced H+ release or [Delta]pH-dependent Ca2+ accumulation. We observed that the amount of Ca2+ taken up by the vesicles increases with the magnitude of the [Delta]pH across the membrane, particularly at Ca2+ concentrations (~500 [mu]M) found optimal for the antiporter activity. Similarly, H+ release induced by Ca2+ increased with the magnitude of [Delta]pH. However, above 60% [Delta]pH (high H+-pump activity), the net H+ release from the vesicles decreased as the pump-mediated H+ influx exceeded the Ca2+-induced H+ efflux. We also observed that the Ca2+/H+ antiport activity depends, essentially, on the [Delta]pH component of the electrochemical gradient (~3 nmol Ca2+ taken up/mg protein), although the [Delta][phi] component may also support some Ca2+ accumulation by the vesicles (~1 nmol/mg protein) in the absence of [Delta]pH. Both Ca2+-induced H+ release and [Delta]pH-dependent Ca2+ uptake could be driven by an artificially imposed proton motive force. Under normal conditions (H+ pump-induced [Delta]pH), the electrochemical gradient dependence of Ca2+ uptake by the vesicles was checked by inhibition of the process with specific inhibitors (bafilomycin A1, ergocryptin, folymicin, DCCD) of the H+-pump activity. These results indicate that synaptic vesicles Ca2+/H+ antiport is indirectly linked to ATP hydrolysis and it is essentially dependent on the chemical component ([Delta]pH) of the electrochemical gradient generated by the H+-pump activity.http://www.sciencedirect.com/science/article/B6T07-3XNK0RN-5/1/35068f0ffa8170fc0d371eb97c98f3bc1999info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleaplication/PDFhttp://hdl.handle.net/10316/5462http://hdl.handle.net/10316/5462https://doi.org/10.1016/S0169-328X(99)00183-7engMolecular Brain Research. 71:2 (1999) 178-184Gonçalves, Paula P.Meireles, Sandra M.Neves, PauloVale, M. Graça P.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:RCAAP2020-11-06T16:59:46Zoai:estudogeral.uc.pt:10316/5462Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T20:55:30.871385Repositório 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 |
Synaptic vesicle Ca2+/H+ antiport: dependence on the proton electrochemical gradient |
title |
Synaptic vesicle Ca2+/H+ antiport: dependence on the proton electrochemical gradient |
spellingShingle |
Synaptic vesicle Ca2+/H+ antiport: dependence on the proton electrochemical gradient Gonçalves, Paula P. Ca2+/H+ antiport Synaptic vesicle Brain cortex |
title_short |
Synaptic vesicle Ca2+/H+ antiport: dependence on the proton electrochemical gradient |
title_full |
Synaptic vesicle Ca2+/H+ antiport: dependence on the proton electrochemical gradient |
title_fullStr |
Synaptic vesicle Ca2+/H+ antiport: dependence on the proton electrochemical gradient |
title_full_unstemmed |
Synaptic vesicle Ca2+/H+ antiport: dependence on the proton electrochemical gradient |
title_sort |
Synaptic vesicle Ca2+/H+ antiport: dependence on the proton electrochemical gradient |
author |
Gonçalves, Paula P. |
author_facet |
Gonçalves, Paula P. Meireles, Sandra M. Neves, Paulo Vale, M. Graça P. |
author_role |
author |
author2 |
Meireles, Sandra M. Neves, Paulo Vale, M. Graça P. |
author2_role |
author author author |
dc.contributor.author.fl_str_mv |
Gonçalves, Paula P. Meireles, Sandra M. Neves, Paulo Vale, M. Graça P. |
dc.subject.por.fl_str_mv |
Ca2+/H+ antiport Synaptic vesicle Brain cortex |
topic |
Ca2+/H+ antiport Synaptic vesicle Brain cortex |
description |
Synaptic vesicles isolated from sheep brain cortex accumulate Ca2+ by a mechanism of secondary active transport associated to the H+-pump activity. The process can be visualized either by measuring Ca2+-induced H+ release or [Delta]pH-dependent Ca2+ accumulation. We observed that the amount of Ca2+ taken up by the vesicles increases with the magnitude of the [Delta]pH across the membrane, particularly at Ca2+ concentrations (~500 [mu]M) found optimal for the antiporter activity. Similarly, H+ release induced by Ca2+ increased with the magnitude of [Delta]pH. However, above 60% [Delta]pH (high H+-pump activity), the net H+ release from the vesicles decreased as the pump-mediated H+ influx exceeded the Ca2+-induced H+ efflux. We also observed that the Ca2+/H+ antiport activity depends, essentially, on the [Delta]pH component of the electrochemical gradient (~3 nmol Ca2+ taken up/mg protein), although the [Delta][phi] component may also support some Ca2+ accumulation by the vesicles (~1 nmol/mg protein) in the absence of [Delta]pH. Both Ca2+-induced H+ release and [Delta]pH-dependent Ca2+ uptake could be driven by an artificially imposed proton motive force. Under normal conditions (H+ pump-induced [Delta]pH), the electrochemical gradient dependence of Ca2+ uptake by the vesicles was checked by inhibition of the process with specific inhibitors (bafilomycin A1, ergocryptin, folymicin, DCCD) of the H+-pump activity. These results indicate that synaptic vesicles Ca2+/H+ antiport is indirectly linked to ATP hydrolysis and it is essentially dependent on the chemical component ([Delta]pH) of the electrochemical gradient generated by the H+-pump activity. |
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 |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10316/5462 http://hdl.handle.net/10316/5462 https://doi.org/10.1016/S0169-328X(99)00183-7 |
url |
http://hdl.handle.net/10316/5462 https://doi.org/10.1016/S0169-328X(99)00183-7 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Molecular Brain Research. 71:2 (1999) 178-184 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
aplication/PDF |
dc.source.none.fl_str_mv |
reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação instacron:RCAAP |
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Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
instacron_str |
RCAAP |
institution |
RCAAP |
reponame_str |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
collection |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
repository.name.fl_str_mv |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
repository.mail.fl_str_mv |
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1799133842193252352 |