GluN2B and GluN2A containing NMDAR are differentially involved in extinction memory destabilization and restabilization during reconsolidation

Radiske, Andressa; Gonzalez, Maria Carolina; Ferreira, Diana Aline Nôga Morais; Rossato, Janine Inez; Bevilaqua, Lia Rejane Müller; Cammarota, Martín Pablo

GluN2B and GluN2A containing NMDAR are differentially involved in extinction memory destabilization and restabilization during reconsolidation

Página do item simplificado Estatísticas

dc.contributor.author	Radiske, Andressa
dc.contributor.author	Gonzalez, Maria Carolina
dc.contributor.author	Ferreira, Diana Aline Nôga Morais
dc.contributor.author	Rossato, Janine Inez
dc.contributor.author	Bevilaqua, Lia Rejane Müller
dc.contributor.author	Cammarota, Martín Pablo
dc.date.accessioned	2021-02-11T16:01:16Z
dc.date.available	2021-02-11T16:01:16Z
dc.date.issued	2021-01-08
dc.description.resumo	Extinction memory destabilized by recall is restabilized through mTOR-dependent reconsolidation in the hippocampus, but the upstream pathways controlling these processes remain unknown. Hippocampal NMDARs drive local protein synthesis via mTOR signaling and may control active memory maintenance. We found that in adult male Wistar rats, intra dorsal-CA1 administration of the non-subunit selective NMDAR antagonist AP5 or of the GluN2A subunit-containing NMDAR antagonist TCN201 after step down inhibitory avoidance (SDIA) extinction memory recall impaired extinction memory retention and caused SDIA memory recovery. On the contrary, pre-recall administration of AP5 or of the GluN2B subunit-containing NMDAR antagonist RO25-6981 had no effect on extinction memory recall or retention per se but hindered the recovery of the avoidance response induced by post-recall intra-CA1 infusion of the mTOR inhibitor rapamycin. Our results indicate that GluN2B-containing NMDARs are necessary for extinction memory destabilization whereas GluN2A-containing NMDARs are involved in its restabilization, and suggest that pharmacological modulation of the relative activation state of these receptor subtypes around the moment of extinction memory recall may regulate the dominance of extinction memory over the original memory trace	pt_BR
dc.identifier.citation	RADISKE, Andressa; GONZALEZ, Maria Carolina; NÔGA, Diana A.; ROSSATO, Janine I.; BEVILAQUA, Lia R. M.; CAMMAROTA, Martín. GluN2B and GluN2A-containing NMDAR are differentially involved in extinction memory destabilization and restabilization during reconsolidation. Scientific Reports, [S. l.], v. 11, n. 1, p. 178-186, 8 jan. 2021. doi:10.1038/s41598-020-80674-7. Disponível em: https://www.nature.com/articles/s41598-020-80674-7. Acesso em: 11 fev. 2021.	pt_BR
dc.identifier.doi	10.1038/s41598-020-80674-7
dc.identifier.uri	https://repositorio.ufrn.br/handle/123456789/31478
dc.language	en	pt_BR
dc.publisher	Springer Science and Business Media LLC	pt_BR
dc.rights	Attribution 3.0 Brazil	*
dc.rights.uri	http://creativecommons.org/licenses/by/3.0/br/	*
dc.subject	GluN2B	pt_BR
dc.subject	GluN2A	pt_BR
dc.subject	NMDAR	pt_BR
dc.subject	Extinction memory	pt_BR
dc.subject	Memory consolidation	pt_BR
dc.subject	Memory	pt_BR
dc.title	GluN2B and GluN2A containing NMDAR are differentially involved in extinction memory destabilization and restabilization during reconsolidation	pt_BR
dc.type	article	pt_BR