Our results show that activation of PPARα and PPARγ (but not PPARδ) reduces ethanol intake and preference in both chronic voluntary and limited access ‘binge’ drinking models in mice with a genetic predisposition for high ethanol consumption. A PPARα agonist reduced ethanol consumption in rats (Barson et al., 2009), and PPARγ agonists reduced ethanol drinking, stress-induced relapse, and withdrawal in alcohol-preferring rats (Stopponi et al., 2011). These effects were not due to changes in blood alcohol levels and were prevented by injection of a selective PPARγ antagonist into the lateral cerebroventricle, showing the importance of central PPARs in mediating reduced alcohol drinking (Stopponi et al., 2011).
