Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/18514
DC FieldValueLanguage
dc.contributor.authorDomingues, António-
dc.contributor.authorCunha-Oliveira, Teresa-
dc.contributor.authorLaço, Mário L. N.-
dc.contributor.authorMacedo, Tice-
dc.contributor.authorOliveira, Catarina R.-
dc.contributor.authorRego, A. Cristina-
dc.date.accessioned2012-03-08T18:39:42Z-
dc.date.available2012-03-08T18:39:42Z-
dc.date.issued2012-03-08-
dc.identifier.urihttp://hdl.handle.net/10316/18514-
dc.description.abstractRepeated use of drugs of abuse, namely opiates, has been shown to affect glutamate-releasing neurons. Moreover, blockade of N-methyl-D-aspartate (NMDA) receptors (NMDAR) prevents cell death by apoptosis induced by morphine, a heroin metabolite. Thus, in this article we investigated the involvement of different NMDAR subunits in heroin cytotoxicity. Human embryonic kidney (HEK293)cells, which do not express native NMDAR, were transfected with NR1/NR2A or NR1/NR2B subunits. As a control, cells were transfected with NR1 alone, which does not form functional channels. Incubation with heroin for 24 h induced a dose-dependent decrease in cell viability both in NR1-transfected and nontransfected cells. The loss of membrane integrity induced by heroin was more evident in cells transfected with NR1/NR2B than in cells transfected with NR1 alone or NR1/NR2A. This decrease in cell viability was blocked by MK-801, a selective and noncompetitive antagonist of NMDAR. Nevertheless, no significant changes in intracellular adenosine 5′-triphosphate (ATP) were observed in cells treated with heroin. These data implicate NR2B-composed NMDAR as important mediators of heroin neurotoxicity.por
dc.language.isoengpor
dc.rightsopenAccesspor
dc.titleExpression of NR1/NR2B N-Methyl-d-Aspartate Receptors Enhances Heroin Toxicity in HEK293 Cellspor
dc.typearticlepor
degois.publication.firstPage458por
degois.publication.lastPage465por
degois.publication.titleAnnals of the New York Academy of Sciencespor
dc.relation.publisherversionhttp://onlinelibrary.wiley.com/doi/10.1196/annals.1369.046/abstractpor
dc.peerreviewedYespor
dc.identifier.doi10.1196/annals.1369.046-
degois.publication.volume1074por
item.grantfulltextopen-
item.fulltextCom Texto completo-
item.openairetypearticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.languageiso639-1en-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.orcid0000-0002-7382-0339-
crisitem.author.orcid0000-0001-6942-4328-
crisitem.author.orcid0000-0003-0700-3776-
Appears in Collections:I&D CNC - Artigos em Revistas Internacionais
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