期刊
JOURNAL OF NEUROCHEMISTRY
卷 137, 期 3, 页码 312-330出版社
WILEY
DOI: 10.1111/jnc.13564
关键词
active demethylation; AMPA receptor; epigenetic; homeostatic plasticity; memory; TET
资金
- NINDS
- NIMH
- NINR
- DARPA
- Pitt-Hopkins Syndrome Foundation
- Civitan International
- Evelyn F. McKnight Brain Research Foundation
Hebbian plasticity, including long-term potentiation and long-term depression, has long been regarded as important for local circuit refinement in the context of memory formation and stabilization. However, circuit development and stabilization additionally relies on non-Hebbian, homeostatic, forms of plasticity such as synaptic scaling. Synaptic scaling is induced by chronic increases or decreases in neuronal activity. Synaptic scaling is associated with cell-wide adjustments in postsynaptic receptor density, and can occur in a multiplicative manner resulting in preservation of relative synaptic strengths across the entire neuron's population of synapses. Both active DNA methylation and demethylation have been validated as crucial regulators of gene transcription during learning, and synaptic scaling is known to be transcriptionally dependent. However, it has been unclear whether homeostatic forms of plasticity such as synaptic scaling are regulated via epigenetic mechanisms. This review describes exciting recent work that has demonstrated a role for active changes in neuronal DNA methylation and demethylation as a controller of synaptic scaling and glutamate receptor trafficking. These findings bring together three major categories of memory-associated mechanisms that were previously largely considered separately: DNA methylation, homeostatic plasticity, and glutamate receptor trafficking.
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