Deleting HDAC3 rescues long-term memory impairments induced by disruption of the neuronspecific chromatin remodeling subunit BAF53b

Guanhua Shu, Enikö A. Kramár, Alberto J. López, Grace Huynh, Marcelo A. Wood, Janine L. Kwapis

Research output: Contribution to journalArticle

9 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)109-114
Number of pages6
JournalLearning and Memory
Volume25
Issue number3
DOIs
StatePublished - Mar 2018

All Science Journal Classification (ASJC) codes

  • Neuropsychology and Physiological Psychology
  • Cognitive Neuroscience
  • Cellular and Molecular Neuroscience

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