Format

Send to

Choose Destination
See comment in PubMed Commons below
Neuropharmacology. 2014 May;80:18-27. doi: 10.1016/j.neuropharm.2013.10.002. Epub 2013 Oct 15.

Neuron-specific chromatin remodeling: a missing link in epigenetic mechanisms underlying synaptic plasticity, memory, and intellectual disability disorders.

Author information

1
University of California, Irvine, Department of Neurobiology & Behavior, Irvine, CA, USA; Center for the Neurobiology of Learning & Memory, Irvine, CA, USA.
2
University of California, Irvine, Department of Neurobiology & Behavior, Irvine, CA, USA; Center for the Neurobiology of Learning & Memory, Irvine, CA, USA. Electronic address: mwood@uci.edu.

Abstract

Long-term memory formation requires the coordinated regulation of gene expression. Until recently nucleosome remodeling, one of the major epigenetic mechanisms for controlling gene expression, had been largely unexplored in the field of neuroscience. Nucleosome remodeling is carried out by chromatin remodeling complexes (CRCs) that interact with DNA and histones to physically alter chromatin structure and ultimately regulate gene expression. Human exome sequencing and gene wide association studies have linked mutations in CRC subunits to intellectual disability disorders, autism spectrum disorder and schizophrenia. However, how mutations in CRC subunits were related to human cognitive disorders was unknown. There appears to be both developmental and adult specific roles for the neuron specific CRC nBAF (neuronal Brg1/hBrm Associated Factor). nBAF regulates gene expression required for dendritic arborization during development, and in the adult, contributes to long-term potentiation, a form of synaptic plasticity, and long-term memory. We propose that the nBAF complex is a novel epigenetic mechanism for regulating transcription required for long-lasting forms of synaptic plasticity and memory processes and that impaired nBAF function may result in human cognitive disorders.

KEYWORDS:

Autism spectrum disorder; Chromatin remodeling; Epigenetics; Intellectual disability disorder; Long-term memory; Long-term potentiation; Nucleosome remodeling

PMID:
24140580
PMCID:
PMC3984593
DOI:
10.1016/j.neuropharm.2013.10.002
[Indexed for MEDLINE]
Free PMC Article

Publication types, MeSH terms, Substances, Grant support

Publication types

MeSH terms

Substances

Grant support

PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center