control, but overexpression did not alter cocaine intake in rats with restricted drug access (Figure 2). The decreased cocaine intake is related to a profound decrease in the motivational properties of the drug, as reflected by a large downward shift in the cocaine dose-response curve in the same animals. Conversely, inhibition of miR-212 signaling in the striatum, achieved by infusion of an antisense oligonucleotide, dramatically increased the motivational properties of cocaine in rats with extended, but not restricted, access to the drug (Figure 2). These data suggest that intrinsic or drug-induce alterations in the expression or activity of striatal miR-212 may influence vulnerability to addiction in human cocaine users.
