The ability to recall the spatial location of objects is crucial for our everyday life. Such memory capability relies on the intricate communication between the hippocampus (HIP) and the medial prefrontal cortex (mPFC), and its decline is often observed with aging. Despite progress in understanding the role of HIP-mPFC communication in object memory, approaches to enhance its functionality are very limited. Therefore, we aimed to explore how optogenetic activation (priming) of the HIP-mPFC pathway can facilitate object-location memory in adult and aging mice. For this purpose, we injected mice with a virus containing an opsin into CA1. We ran two control groups to account for the mere effect of the light and the opsin, respectively. First, we tested the response of mPFC neurons to optogenetic stimulation of HIP terminals in ex-vivo electrophysiology. Here, we confirmed that we can induce an oEPSP in postsynaptic mPFC neurons. Next, we optogenetically primed the HIP efferents in the mPFC prior to running the initial object-in-place (OIP) task to assess behavioral effects on recognition performance. The OIP task was repeated two times without priming. Primed mice showed significantly higher performance than controls (t-test, p<0.05) in the first test. Over the tests primed mice had a steady performance, while control groups improved over the tests (repeated ANOVA, p<0.05). Our results indicate that object location recognition memory relies on the strength of the HIP-mPFC network, which can be enhanced artificially through optogenetic stimulation of HIP-PFC projections. Now, we are using in-vivo electropohyioslogy to further investigate the mechanism.