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MeCP2 controls BDNF expression and cocaine intake through homeostatic interactions with microRNA-212.

Authors: Im, Heh-In  Hollander, Jonathan A  Bali, Purva  Kenny, Paul J 
Citation: Im HI, etal., Nat Neurosci. 2010 Sep;13(9):1120-7. doi: 10.1038/nn.2615. Epub 2010 Aug 15.
Pubmed: (View Article at PubMed) PMID:20711185
DOI: Full-text: DOI:10.1038/nn.2615

The X-linked transcriptional repressor methyl CpG binding protein 2 (MeCP2), known for its role in the neurodevelopmental disorder Rett syndrome, is emerging as an important regulator of neuroplasticity in postmitotic neurons. Cocaine addiction is commonly viewed as a disorder of neuroplasticity, but the potential involvement of MeCP2 has not been explored. Here we identify a key role for MeCP2 in the dorsal striatum in the escalating cocaine intake seen in rats with extended access to the drug, a process that mimics the increasingly uncontrolled cocaine use seen in addicted humans. MeCP2 regulates cocaine intake through homeostatic interactions with microRNA-212 (miR-212) to control the effects of cocaine on striatal brain-derived neurotrophic factor (BDNF) levels. These data suggest that homeostatic interactions between MeCP2 and miR-212 in dorsal striatum may be important in regulating vulnerability to cocaine addiction.


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CRRD Object Information
CRRD ID: 12789445
Created: 2017-02-14
Species: All species
Last Modified: 2017-02-14
Status: ACTIVE


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