Abstract
The establishment of synaptic plasticity and long-term memory requires lasting cellular and molecular modifications that, as a whole, must endure despite the rapid turnover of their constituent parts. Such a molecular feat must be mediated by a stable, self-perpetuating, cellular information storage mechanism. DNA methylation, being the archetypal cellular information storage mechanism, has been heavily implicated as being necessary for stable activity-dependent transcriptional alterations within the CNS. This review details the foundational discoveries from both gene-targeted and whole-genome sequencing studies that have brought DNA methylation to our attention as a chief regulator of activity- and experience-dependent transcriptional alterations within the CNS. We present a hypothetical framework to resolve disparate experimental findings regarding distinct manipulations of DNA methylation and their effect on memory, taking into account the unique impact activity-dependent alterations in DNA methylation potentially have on both memory-promoting and memory-suppressing gene expression. And last, we discuss potential avenues for future inquiry into the role of DNA methylation during remote memory formation.
Original language | English (US) |
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Pages (from-to) | 475-489 |
Number of pages | 15 |
Journal | Neuroscientist |
Volume | 21 |
Issue number | 5 |
DOIs | |
State | Published - Oct 30 2015 |
Externally published | Yes |
Keywords
- DNA demethylation
- DNA methylation
- epigenetics
- memory
- synaptic plasticity
ASJC Scopus subject areas
- General Neuroscience
- Clinical Neurology