Naloxone inhibits nicotine-induced receptor current and catecholamine secretion in bovine chromaffin cells
Autor(a) principal: | |
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Data de Publicação: | 2001 |
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/10316/3886 https://doi.org/10.1016/S0006-8993(01)02388-5 |
Resumo: | Nicotine-induced catecholamine (CA) secretion and inward ionic currents were inhibited by the opioid antagonist naloxone in cultured bovine chromaffin cells. Naloxone inhibited nicotine-induced CA secretion, as detected by an on-line real-time electrochemical technique, in a dose-dependent manner (IC50=29 [mu]M). In voltage-clamped chromaffin cells, nicotine (10 [mu]M) evoked an average peak inward current of -146 pA that was inhibited by low concentrations of naloxone (42% at 0.1 [mu]M). The antagonist also inhibited total charge influx associated with nicotinic receptor activation (53% at 0.1 [mu]M). This provides strong evidence that naloxone modulation of nicotine-induced CA secretion does not involve opioid receptors but results from the direct interaction with the nicotinic receptor itself, which might also be the case for other related opioid compounds. |
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Naloxone inhibits nicotine-induced receptor current and catecholamine secretion in bovine chromaffin cellsOpioidsNicotinic receptorCurrentsCatecholamine secretionPatch-clampNicotine-induced catecholamine (CA) secretion and inward ionic currents were inhibited by the opioid antagonist naloxone in cultured bovine chromaffin cells. Naloxone inhibited nicotine-induced CA secretion, as detected by an on-line real-time electrochemical technique, in a dose-dependent manner (IC50=29 [mu]M). In voltage-clamped chromaffin cells, nicotine (10 [mu]M) evoked an average peak inward current of -146 pA that was inhibited by low concentrations of naloxone (42% at 0.1 [mu]M). The antagonist also inhibited total charge influx associated with nicotinic receptor activation (53% at 0.1 [mu]M). This provides strong evidence that naloxone modulation of nicotine-induced CA secretion does not involve opioid receptors but results from the direct interaction with the nicotinic receptor itself, which might also be the case for other related opioid compounds.http://www.sciencedirect.com/science/article/B6SYR-43MC9YT-C/1/1994796a9d2862757ab52186bcacc5f62001info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleaplication/PDFhttp://hdl.handle.net/10316/3886http://hdl.handle.net/10316/3886https://doi.org/10.1016/S0006-8993(01)02388-5engBrain Research. 903:1-2 (2001) 62-65Tomé, Ângelo R.Izaguirre, VictorRosário, Luís M.Ceña, ValentínGonzález-García, Carmeninfo: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:RCAAP2021-11-04T11:02:18Zoai:estudogeral.uc.pt:10316/3886Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T20:55:43.203326Repositório 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 |
Naloxone inhibits nicotine-induced receptor current and catecholamine secretion in bovine chromaffin cells |
title |
Naloxone inhibits nicotine-induced receptor current and catecholamine secretion in bovine chromaffin cells |
spellingShingle |
Naloxone inhibits nicotine-induced receptor current and catecholamine secretion in bovine chromaffin cells Tomé, Ângelo R. Opioids Nicotinic receptor Currents Catecholamine secretion Patch-clamp |
title_short |
Naloxone inhibits nicotine-induced receptor current and catecholamine secretion in bovine chromaffin cells |
title_full |
Naloxone inhibits nicotine-induced receptor current and catecholamine secretion in bovine chromaffin cells |
title_fullStr |
Naloxone inhibits nicotine-induced receptor current and catecholamine secretion in bovine chromaffin cells |
title_full_unstemmed |
Naloxone inhibits nicotine-induced receptor current and catecholamine secretion in bovine chromaffin cells |
title_sort |
Naloxone inhibits nicotine-induced receptor current and catecholamine secretion in bovine chromaffin cells |
author |
Tomé, Ângelo R. |
author_facet |
Tomé, Ângelo R. Izaguirre, Victor Rosário, Luís M. Ceña, Valentín González-García, Carmen |
author_role |
author |
author2 |
Izaguirre, Victor Rosário, Luís M. Ceña, Valentín González-García, Carmen |
author2_role |
author author author author |
dc.contributor.author.fl_str_mv |
Tomé, Ângelo R. Izaguirre, Victor Rosário, Luís M. Ceña, Valentín González-García, Carmen |
dc.subject.por.fl_str_mv |
Opioids Nicotinic receptor Currents Catecholamine secretion Patch-clamp |
topic |
Opioids Nicotinic receptor Currents Catecholamine secretion Patch-clamp |
description |
Nicotine-induced catecholamine (CA) secretion and inward ionic currents were inhibited by the opioid antagonist naloxone in cultured bovine chromaffin cells. Naloxone inhibited nicotine-induced CA secretion, as detected by an on-line real-time electrochemical technique, in a dose-dependent manner (IC50=29 [mu]M). In voltage-clamped chromaffin cells, nicotine (10 [mu]M) evoked an average peak inward current of -146 pA that was inhibited by low concentrations of naloxone (42% at 0.1 [mu]M). The antagonist also inhibited total charge influx associated with nicotinic receptor activation (53% at 0.1 [mu]M). This provides strong evidence that naloxone modulation of nicotine-induced CA secretion does not involve opioid receptors but results from the direct interaction with the nicotinic receptor itself, which might also be the case for other related opioid compounds. |
publishDate |
2001 |
dc.date.none.fl_str_mv |
2001 |
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/10316/3886 http://hdl.handle.net/10316/3886 https://doi.org/10.1016/S0006-8993(01)02388-5 |
url |
http://hdl.handle.net/10316/3886 https://doi.org/10.1016/S0006-8993(01)02388-5 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Brain Research. 903:1-2 (2001) 62-65 |
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 |
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RCAAP |
institution |
RCAAP |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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