One of the most fascinating properties of the brain is its ability to adjust behaviors, which typically results from experience-dependent modifications of neuronal circuits. Synaptic plasticity refers to changes in synaptic strength at pre-existing synapses induced by transient activity. By modifying neural circuit flow, synaptic plasticity is believed to play a central role in the capacity of the brain to incorporate new experiences into persistent memories. Long-term potentiation has emerged as a prominent mechanism associated with learning and memory. Protein synthesis is well-recognized as a key mediator of synaptic efficacy, neuronal connectivity, and activity-dependent plasticity. The dentate gyrus, a region located in the hippocampus, is involved in memory formation. Within the dentate gyrus, dentate granule cells (GCs) receive excitatory inputs from the entorhinal cortex through the medial and lateral perforant paths. Previous work reported that the synapse established between MPP and GC (MPP-GC) can undergo LTP in vivo. While protein synthesis seems to be required for MPP-GC LTP, the precise mechanisms that control MPP-GC LTP remain unknown. Therefore, the objective of my project is to investigate the requirement of protein synthesis for LTP at the MPP-GC synapse. To do so, we used slice electrophysiology and tested the effects of inhibitors of protein synthesis in MPP-GC LTP. By utilizing extracellular recordings, we showed that tetanic stimulation induces LTP at MPP-GC synapses, and this plasticity was abolished in the presence of anisomycin. Altogether, our preliminary data demonstrated that MPP-GC synapses can undergo LTP, and protein synthesis is required for this plasticity.