molecular and behavioral deficits were rescued via specific knockdown of HDAC2 expression either by direct infusion of small interfering RNA (siRNA) against HDAC2 into the central AMG nucleus (61, 66) or by TSA treatment (127, 130, 132). Collectively, these observations raised the possibility that adaptive epigenetic changes involving HDACs, and in particular HDAC2, in the AMG may be important regulatory mechanisms that underlie expression of genes implicated in the development and pathogenesis of alcohol dependence.
