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. Author manuscript; available in PMC: 2018 Dec 1.
Published in final edited form as: Biol Psychiatry. 2017 May 5;82(11):794–805. doi: 10.1016/j.biopsych.2017.04.013

Figure 6.

Figure 6

Model for cocaine regulation of the 3D genome in NAc. 3C/4C demonstrate that Auts2 and Caln1 form a loop, which is disrupted by repeated cocaine. CTCF, a mediator of looping, binds less to Auts2 and Caln1 after cocaine administration, with coincident increases in the permissive chromatin mark, H3K4me3. We propose that these changes are mediated by increased DNA methylation at a CTCF site and lead to opening of the Auts2-Caln1 loop, which mediates the cocaine-induced increase in their expression. Such induction of Auts2 and Caln1 then augments rewarding responses to cocaine. These mechanisms appear specific for NAc D2 MSNs.