Deleting HDAC3 rescues long-term memory impairments induced by disruption of the neuron-specific chromatin remodeling subunit BAF53b.
Learn Mem
; 25(3): 109-114, 2018 03.
Article
em En
| MEDLINE
| ID: mdl-29449454
ABSTRACT
Multiple epigenetic mechanisms, including histone acetylation and nucleosome remodeling, are known to be involved in long-term memory formation. Enhancing histone acetylation by deleting histone deacetylases, like HDAC3, typically enhances long-term memory formation. In contrast, disrupting nucleosome remodeling by blocking the neuron-specific chromatin remodeling subunit BAF53b impairs long-term memory. Here, we show that deleting HDAC3 can ameliorate the impairments in both long-term memory and synaptic plasticity caused by BAF53b mutation. This suggests a dynamic interplay exists between histone acetylation/deacetylation and nucleosome remodeling mechanisms in the regulation of memory formation.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Potenciação de Longa Duração
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Memória de Longo Prazo
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Histona Desacetilases
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Transtornos da Memória
Limite:
Animals
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article