Systemic administration of dopamine D1-like (SCH23390) and, to a lesser degree D2-like (raclopride), receptor antagonists significantly reduce the acquisition and expression of fructose-conditioned flavor preferences (CFP) in rats. Given the role of dopamine in the amygdala (AMY) in the processing and learning of food reward, the present study examined whether dopamine D1-like or D2-like antagonists in this site altered acquisition and/or expression of a fructose-CFP. In Experiment 1, food-restricted rats with bilateral AMY cannulae were trained to drink a fructose (8%) + saccharin (0.2%) solution mixed with one flavor (e.g., grape, CS+/Fs) and a less-preferred 0.2% saccharin solution mixed with another flavor (e.g., cherry, CS−/s) during one-bottle (16 ml) sessions. Two-bottle tests with the two flavors mixed in saccharin solutions (CS+/s, CS−/s) occurred 10 min following total bilateral AMY doses of 0, 12, 24 and 48 nmol of SCH23390 or raclopride. Preference for CS+/s over CS−/s was significantly reduced relative to vehicle baseline by the 48 nmol doses of SCH23390 and raclopride (from 77% to 66% and 68%), but not lower doses. In Experiment 2, rats received bilateral AMY injections (12 nmol) of SCH23390 (D1 group) or raclopride (D2 group) 10 min prior to one-bottle training sessions with CS+/Fs and CS−/s. Yoked Control rats received vehicle and were limited to the CS intakes of the D1 and D2 groups; untreated controls were not injected or limited to drug group intakes during training. Subsequent two-bottle tests revealed initial preferences of CS+/s over CS−/s in all groups that remained stable in untreated and Yoked Controls, but were lost over the 6 tests sessions in the D1 group, but not in the D2 group. These data indicate that dopamine D1-like and D2-like antagonists significantly attenuated the expression of the previously acquired fructose-CFP, and did not block acquisition of the fructose-CFP. D1-like antagonism during training hastened extinction of the fructose-CFP. The results are similar to those produced by dopamine D1-like and D2-like antagonist injections into the nucleus accumbens shell which suggests that flavor conditioning involves a regionally distributed brain network.