Essential Role of the Histone Methyltransferase G9a in Cocaine-Induced Plasticity
Herbert E. Covington, III1,
David M. Dietz1,
Scott J. Russo1,
Rachael L. Neve3,
Stephen J. Haggarty4,5,
Srihari C. Sampath6,
Yasmin L. Hurd1,
Anne Schaefer7, and
Eric J. Nestler1,*
1 Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY, USA.
2 Departments of Psychiatry and Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX, USA.
3 Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.
4 Psychiatric and Neurodevelopmental Genetics Unit and Molecular Neurogenetics Unit, Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA, USA.
5 Stanley Center for Psychiatric Research, Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA, USA.
6 Laboratory of Lymphocyte Signaling, The Rockefeller University, New York, NY, USA.
7 Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY, USA.
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Fig. 2. G9a in NAc regulates cocaine-induced behavioral plasticity. (A) Representative image of HSV-mediated transgene expression in the NAc. The cartoon of the coronal brain slice was taken from the mouse brain atlas. (B) Conditioned place preference for cocaine and (C) H3K9me2 levels in the NAc in animals infected with HSV-GFP, HSV-G9a, or HSV-G9aH1093K. (D) Conditioned place preference for cocaine and (E) H3K9me2 levels in the NAc in G9afl/fl animals infected with AAV-GFP or AAV-Cre. (F) Conditioned place preference for cocaine and (G) H3K9me2 levels in the NAc in animals receiving intra-NAc vehicle or BIX01294. Data are presented as mean ± SEM.|