Please use this identifier to cite or link to this item:
https://hdl.handle.net/10316/109425
DC Field | Value | Language |
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dc.contributor.author | Zappettini, Stefania | - |
dc.contributor.author | Grilli, Massimo | - |
dc.contributor.author | Olivero, Guendalina | - |
dc.contributor.author | Chen, Jiayang | - |
dc.contributor.author | Padolecchia, Cristina | - |
dc.contributor.author | Pittaluga, Anna | - |
dc.contributor.author | Tomé, Ângelo R. | - |
dc.contributor.author | Cunha, Rodrigo A. | - |
dc.contributor.author | Marchi, Mario | - |
dc.date.accessioned | 2023-10-13T10:56:46Z | - |
dc.date.available | 2023-10-13T10:56:46Z | - |
dc.date.issued | 2014 | - |
dc.identifier.issn | 1662-5102 | pt |
dc.identifier.uri | https://hdl.handle.net/10316/109425 | - |
dc.description.abstract | We here provide functional and immunocytochemical evidence supporting the co-localization and functional interaction between nicotinic acetylcholine receptors (nAChRs) and N-methyl-D-aspartic acid receptors (NMDARs) in glutamatergic terminals of the nucleus accumbens (NAc). Immunocytochemical studies showed that a significant percentage of NAc terminals were glutamatergic and possessed GluN1 and α7-containing nAChR. A short-term pre-exposure of synaptosomes to nicotine (30 µM) or choline (1 mM) caused a significant potentiation of the 100 µM NMDA-evoked [(3)H]D-aspartate ([(3)H]D-Asp) outflow, which was prevented by α-bungarotoxin (100 nM). The pre-exposure to nicotine (100 µM) or choline (1 mM) also enhanced the NMDA-induced cytosolic free calcium levels, as measured by FURA-2 fluorescence imaging in individual NAc terminals, an effect also prevented by α-bungarotoxin. Pre-exposure to the α4-nAChR agonists 5IA85380 (10 nM) or RJR2429 (1 µM) did not modify NMDA-evoked ([(3)H]D-Asp) outflow and calcium transients. The NMDA-evoked ([(3)H]D-Asp) overflow was partially antagonized by the NMDAR antagonists MK801, D-AP5, 5,7-DCKA and R(-)CPP and unaffected by the GluN2B-NMDAR antagonists Ro256981 and ifenprodil. Notably, pre-treatment with choline increased GluN2A biotin-tagged proteins. In conclusion, our results show that the GluN2A-NMDA receptor function can be positively regulated in NAc terminals in response to a brief incubation with α7 but not α4 nAChRs agonists. This might be a general feature in different brain areas since a similar nAChR-mediated bolstering of NMDA-induced ([(3)H]D-Asp) overflow was also observed in hippocampal synaptosomes. | pt |
dc.language.iso | eng | pt |
dc.publisher | Frontiers Media S.A. | pt |
dc.relation | ThisworkwassupportedbyItalianMIURtoMarioMarchi(Prot. N 2009R7WCZS_003),byUniversityofGenoa“Athenaeum ResearchProject”.WewishtothankMauraAgateandDr.Silvia E. Smith,Ph.D(UniversityofIdaho,IBEST,SchoolofLife Sciences)foreditorialassistance.RodrigoA.CunhaandAngelo R. ToméweresupportedbyQREN(CENTRO-07-ST24-FEDER- 002006), FundaçãoparaaCiênciaeaTecnologia(PTDC/SAU- NSC/122254/2010) andtheU.S.ArmyResearchOfficeandthe DefenseAdvancedResearchProjectsAgency(grantW911NF-10- 1-0059) | pt |
dc.rights | openAccess | pt |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | pt |
dc.subject | nicotinic receptors | pt |
dc.subject | NMDA receptors | pt |
dc.subject | nicotine treatment | pt |
dc.subject | neurotransmitters release | pt |
dc.subject | synaptosomes | pt |
dc.subject | nucleus accumbens | pt |
dc.title | Nicotinic α7 receptor activation selectively potentiates the function of NMDA receptors in glutamatergic terminals of the nucleus accumbens | pt |
dc.type | article | - |
degois.publication.firstPage | 332 | pt |
degois.publication.issue | OCT | pt |
degois.publication.title | Frontiers in Cellular Neuroscience | pt |
dc.peerreviewed | yes | pt |
dc.identifier.doi | 10.3389/fncel.2014.00332 | pt |
degois.publication.volume | 8 | pt |
dc.date.embargo | 2014-01-01 | * |
uc.date.periodoEmbargo | 0 | pt |
item.grantfulltext | open | - |
item.cerifentitytype | Publications | - |
item.languageiso639-1 | en | - |
item.openairetype | article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | Com Texto completo | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.orcid | 0000-0001-8671-989X | - |
crisitem.author.orcid | 0000-0003-2550-6422 | - |
Appears in Collections: | FMUC Medicina - Artigos em Revistas Internacionais FCTUC Ciências da Vida - Artigos em Revistas Internacionais I&D CNC - Artigos em Revistas Internacionais |
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Nicotinic α7 receptor activation selectively potentiates the function of NMDA receptors in glutamatergic terminals of the nucleus accumbens.pdf | 1.31 MB | Adobe PDF | View/Open |
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