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. Author manuscript; available in PMC: 2010 Jul 8.
Published in final edited form as: Science. 2010 Jan 8;327(5962):213. doi: 10.1126/science.1179438

Fig. 1.

Fig. 1

Repeated cocaine represses G9a expression in NAc through a ΔFosB-dependent mechanism. (A) mRNA expression of H3K9/K27 KMTs and KDMs in NAc 24 hr after repeated cocaine. (B) H3K9me2 levels in NAc 24 hr after repeated cocaine. (C) Analysis of gene expression after acute or repeated cocaine. Heatmaps (*) show genes upregulated in NAc 1 hr after a cocaine challenge in naïve animals (Acute), in animals treated repeatedly with cocaine (Repeated + acute) or in animals after 168 hr withdrawal from repeated cocaine (Repeated wd + acute). Associated heatmaps show how genes were affected under the other 2 conditions. Desensitized transcriptional responses following repeated cocaine are indicated (***). (D) H3K9me2 levels in NAc from NSE-tTA × tetOP-ΔFosB mice on (‘Δ FosB off’) or off (‘Δ FosB on’) doxycycline 1 hr after repeated cocaine. (E) G9a mRNA expression in NAc from NSE-tTA × tetOP-ΔFosB mice on (‘Δ FosB off’) and off (‘Δ FosB on’) doxycycline, and from mice infected with AAV-GFP or AAV-ΔFosB. Data are presented as mean ± SEM. For statistical analyses, see full figure legends in “supporting online text.”