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https://hdl.handle.net/10316/109425
Título: | Nicotinic α7 receptor activation selectively potentiates the function of NMDA receptors in glutamatergic terminals of the nucleus accumbens | Autor: | Zappettini, Stefania Grilli, Massimo Olivero, Guendalina Chen, Jiayang Padolecchia, Cristina Pittaluga, Anna Tomé, Ângelo R. Cunha, Rodrigo A. Marchi, Mario |
Palavras-chave: | nicotinic receptors; NMDA receptors; nicotine treatment; neurotransmitters release; synaptosomes; nucleus accumbens | Data: | 2014 | Editora: | Frontiers Media S.A. | Projeto: | 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) | Título da revista, periódico, livro ou evento: | Frontiers in Cellular Neuroscience | Volume: | 8 | Número: | OCT | Resumo: | 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. | URI: | https://hdl.handle.net/10316/109425 | ISSN: | 1662-5102 | DOI: | 10.3389/fncel.2014.00332 | Direitos: | openAccess |
Aparece nas coleções: | 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 | Ver/Abrir |
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