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Because of D2Rs role in the activation of DAT, the association between reduced D2R expression and alcohol consumption supports the possibility of a similar relationship between alcohol consumption and DAT expression ( DAT1 promoter, resulting in the upregulation of DAT in a variety of brain regions ( DAT1 promoter ( While this evidence is still inconclusive, the possible hypermethylation of DAT1 by chronic ethanol consumption would be consistent with the decreased mesolimbic DA release associated with chronic drinking ( DAT1 hypermethylation and decreased DAT expression could serve as a compensatory mechanism to maintain extracellular dopamine levels by decreasing synaptic reuptake ( As a stressor, acute alcohol consumption induces glucocorticoid secretion, which increases the level of cortisol in the blood ( H of NR3C1 , which encodes GR, in postmortem brain tissue of human AUD subjects compared to controls ( via methylation of NR3C1

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