The frontal association cortex (FrA) is implicated in higher brain function. Inactivation of the FrA is known to impair the formation of associative memory. The dendritic spine remodeling in FrA neurons occurs in response to paired sensory stimuli that produce associative memory. However, the precise role of the FrA during associative learning remains unclear. Here, we find stimulus integration in the FrA during associative learning. First, we examined whether the FrA is required for memory formation in contextual fear conditioning of the mouse. Pre-conditioning infusion of AP5, an NMDA receptor antagonist, or post-conditioning infusion of anisomycin, a protein synthesis inhibitor, into the FrA reduced freezing behavior in the subsequent test sessions. To visualize stimulus convergence, we employed Arc cellular compartment analysis of temporal activity by fluorescent in situ hybridization (catFISH). We experimentally separated contextual fear conditioning into context exposure and shock and found that both stimuli trigger activity-dependent gene expression in the FrA. A subset of FrA neurons were activated by both stimuli. We also discovered that infusion of anisomycin into the FrA after context exposure disrupted freezing behavior and after shock as well. Thus, protein synthesis in the FrA associated with both context and shock were required for memory formation. Furthermore, we found that the FrA receives the projections from perirhinal and insular cortices, which are implicated in context and shock encoding, respectively. Perirhinal and insular neurons projecting to the FrA participated in contextual fear learning. These findings indicate that the FrA is engaged in stimulus integration and contributes to memory formation in associative learning.