| First Author | Shu G | Year | 2018 |
| Journal | Learn Mem | Volume | 25 |
| Issue | 3 | Pages | 109-114 |
| PubMed ID | 29449454 | Mgi Jnum | J:273932 |
| Mgi Id | MGI:6282936 | Doi | 10.1101/lm.046920.117 |
| Citation | Shu G, et al. (2018) Deleting HDAC3 rescues long-term memory impairments induced by disruption of the neuron-specific chromatin remodeling subunit BAF53b. Learn Mem 25(3):109-114 |
| abstractText | 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. |
