Class I HDAC inhibition improves object recognition memory consolidation through BDNF/TrkB pathway in a time-dependent manner


Por: Ramirez-Mejia, Gerardo, Gil-Lievana, Elvi, Urrego-Morales, Oscar, Soto-Reyes, Ernesto, Bermudez-Rattoni, Federico

Publicada: 1 abr 2021
Resumen:
There is increasing evidence showing that HDACs regulates BDNF (brain-derived neurotrophic factor) expression through its interaction with the Bdnf gene promoter, a key regulator to consolidate memory. Although the nuclear mechanisms regulated by HDACs that control BDNF expression have been partially described recently, the temporal events for memory consolidation remain unknown. Hence, in this work, we studied the temporal pattern for the activation of the BDNF/TrkB pathway through class I HDAC inhibition to enhance object recognition memory (ORM) consolidation. To this end, we inhibited class I HDAC into the insular cortex (IC) and a weak ORM protocol was used to assess temporal expression and function of the BDNF/TrkB pathway in the IC. We found that cortical class I HDAC inhibition enhanced long-term ORM, coincident with a clear peak of BDNF expression at 4 h after acquisition. Furthermore, the tyrosine kinase B (TrkB) receptor blockade at 4 h, but not at 8 h, impaired the consolidation of ORM. These results suggest that histone acetylation regulates the temporal expression of BDNF in cortical circuits potentiating the long-term recognition memory.

Filiaciones:
Ramirez-Mejia, Gerardo:
 División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México04510, Mexico

Gil-Lievana, Elvi:
 División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México04510, Mexico

Urrego-Morales, Oscar:
 División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México04510, Mexico

Soto-Reyes, Ernesto:
 Departamento de Ciencias Naturales, Universidad Autónoma Metropolitana, Unidad Cuajimalpa, 05348, Mexico

Bermudez-Rattoni, Federico:
 División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México04510, Mexico
ISSN: 00283908





Neuropharmacology
Editorial
Elsevier Ltd, THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND, Reino Unido
Tipo de documento: Article
Volumen: 187 Número:
Páginas:
WOS Id: 000631250300001
ID de PubMed: 33581144

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