It is now known that multiple forms of forgetting exist, some of which are active processes. Anderson et al. in 1994 postulated that the act of remembering some experiences causes the forgetting of others. Work in our lab has extended this finding by demonstrating an analogous phenomenon in rats. This retrieval-induced forgetting (RIF) is understood to be a competition-dependent, cue-independent process, driven by prefrontal inhibitory control signals that target the areas where memories are stored. Separate lines of evidence from our lab have shown that the serotonin 2a receptor (5-HT2AR) and the dopamine d1/5 receptor (D1/5R) in the mPFC are each necessary for RIF. It is unclear whether these receptors function independently or interact to produce RIF. This work aims to determine the existence and mechanism of a functional interaction between these receptors in RIF. We conducted a disconnection experiment that revealed that RIF was impaired when antagonists for each receptor were administered in opposite hemispheres, but was unaffected when both were applied unilaterally. The abolition of RIF produced by 5-HT2AR antagonism is reversed by a D1/5R agonist. In summary, our results identify a functional interaction between 5-HT2AR and D1/5R as a mechanism underlying retrieval-induced forgetting and opens new avenues for investigating how modulatory signals in the PFC are leveraged to resolve memory competition and adaptive behavior.