Chunk #24 — Introduction — 1. Epigenetic Regulation due to Histone Covalent Modifications — 1E. Other Drugs of Abuse and Histone Acetylation and Deacetylation Mechanisms
Addiction mechanisms are conserved at the neuroanatomic and molecular level and so understanding the basis of acetylation and deacetylation mechanisms that regulate other drugs of abuse (e.g. cocaine) phenotypes gives us a clue as to which neuroanatomic regions and underlying molecular pathways are shared mechanisms among these different classes of drugs with addictive potential (Robison & Nestler, 2011). CREB and corticotropin releasing factor interactions have been implicated in stress-induced cocaine reward potentiation (Kreibich et al., 2009). CBP-mediated acetylation has also been shown to regulate cocaine behaviors. For example, mice that are haploinsufficient for CBP show decreased sensitivity to cocaine, due to decreased histone acetylation at the fosB promoter (Levine et al., 2005). Cocaine was shown to induce c-fos expression and increase acetylation at the c-fos promoter, which were reduced in a CBP focal knockout in the NAc that also reduced cocaine sensitivity (Malvaez, Mhillaj, Matheos, Palmery, & Wood, 2011). Acute cocaine was shown to rapidly induce H4 acetylation, but not H3, at the cFos promoter, whereas chronic cocaine administration induced histone H3 acetylation at the BDNF promoter (Kumar et al.,
