Evidence suggests that meal-related memory influences later eating behavior. Memory can serve as a powerful mechanism for controlling eating behavior because it provides a record of recent intake that likely outlasts most physiological signals generated by ingestion. Dorsal (dHC) and ventral hippocampal (vHC) neurons are critical for memory, and we demonstrated previously that they limit energy intake during the postprandial period. If dHC or vHC neurons control intake through a process that requires memory, then ingestion should increase events necessary for synaptic plasticity in dHC and vHC during the postprandial period. To test this, we determined whether ingesting a sucrose solution induced posttranslational events critical for hippocampal synaptic plasticity: phosphorylation of AMPAR GluA1 subunits at 1) serine 831 (pSer) and 2) serine 845 (pSer). We also examined whether increasing the amount of previous experience with the sucrose solution, which would be expected to decrease the mnemonic demand involved in an ingestion bout, would also attenuate sucrose-induced phosphorylation. Quantitative immunoblotting of dHC and vHC membrane fractions demonstrated that sucrose ingestion increased postprandial pSer in dHC but not vHC. Increased previous sucrose experience prevented sucrose-induced dHC pSer. Sucrose ingestion did not affect pSer in either dHC or vHC. Thus, the present findings show that ingestion activates a postranslational event necessary for synaptic plasticity in an experience-dependent manner, which is consistent with the hypothesis that dHC neurons form a memory of a meal during the postprandial period.