Memory consolidation is an essential process for our everyday lives. Memory representations are initially encoded in the hippocampus before being consolidated in the neocortex by synaptic plasticity processes that depend on protein synthesis. Within prefrontal cortex (PFC), inhibitory interneurons are critical in gating incoming hippocampal inputs and shaping pyramidal neuron responses. However, how molecular pathways affect synaptic signaling during memory consolidation is unclear. We hypothesize that mechanistic Target Of Rapamycin Complex 1 (mTORC1), a central regulator of protein synthesis, plays an essential role in inhibitory signalling between the hippocampus and the prefrontal cortex. To test this hypothesis, we first evaluated the role of mTORC1 in memory consolidation using a PFC-dependent spatial object recognition task. We found that infusion of rapamycin, a selective mTORC1 inhibitor, into the PFC immediately but not 3 hours after training disrupted long-term memory expression. Then, we evaluated the role of different prefrontal inhibitory interneurons during memory consolidation. We observed that chemogenetic inactivation of parvalbumin-positive (PV) but not of somatostatin-positive interneurons (SOM) after training enhanced memory performance. Finally, we assessed the effect of silencing mTORC1 in different interneuronal subclasses using shRNA strategies. We found that specific mTORC1 downregulation in PV but not SOM interneurons led to long-term memory expression impairments. Overall, our results suggest a key role of mTORC1 in controlling prefrontal inhibitory interneuron plasticity.