1. Universidade Federal do Rio Grande do Norte
2. Instituto do Cérebro
3. ICe - Artigos publicados em periódicos

Título:	GluN2B and GluN2A containing NMDAR are differentially involved in extinction memory destabilization and restabilization during reconsolidation
Autor(es):	Radiske, Andressa Gonzalez, Maria Carolina Ferreira, Diana Aline Nôga Morais Rossato, Janine Inez Bevilaqua, Lia Rejane Müller Cammarota, Martín Pablo
Palavras-chave:	GluN2B;GluN2A;NMDAR;Extinction memory;Memory consolidation;Memory
Data do documento:	8-Jan-2021
Editor:	Springer Science and Business Media LLC
Referência:	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.
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
URI:	https://repositorio.ufrn.br/handle/123456789/31478
Aparece nas coleções:	ICe - Artigos publicados em periódicos

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