Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

The Rett syndrome protein MeCP2 regulates synaptic scaling.

Authors: Qiu, Zilong  Sylwestrak, Emily L  Lieberman, David N  Zhang, Yan  Liu, Xin-Yu  Ghosh, Anirvan 
Citation: Qiu Z, etal., J Neurosci. 2012 Jan 18;32(3):989-94. doi: 10.1523/JNEUROSCI.0175-11.2012.
Pubmed: (View Article at PubMed) PMID:22262897
DOI: Full-text: DOI:10.1523/JNEUROSCI.0175-11.2012

Synaptic scaling is a form of homeostatic synaptic plasticity characterized by cell-wide changes in synaptic strength in response to changes in overall levels of neuronal activity. Here we report that bicuculline-induced increase in neuronal activity leads to a decrease in mEPSC amplitude and a decrease in expression of the AMPA receptor subunit GluR2 in rat hippocampal cultures. Bicuculline treatment also leads to an increase in the levels of the transcriptional repressor MeCP2, which binds to the GluR2 promoter along with the corepressors HDAC1 and mSin3A. Downregulation of MeCP2 by shRNA expression or genetic deletion blocks the bicuculline-induced decrease in GluR2 expression and mEPSC amplitude. These observations indicate that MeCP2 mediates activity-dependent synaptic scaling, and suggest that the pathophysiology of Rett syndrome, which is caused by mutations in MeCP2, may involve defects in activity-dependent regulation of synaptic currents.

Annotation

Gene Ontology Annotations
Objects Annotated

Additional Information

 
CRRD Object Information
CRRD ID: 12790719
Created: 2017-02-21
Species: All species
Last Modified: 2017-02-21
Status: ACTIVE



NHLBI Logo

RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.