Because KORs are expressed in moderately high levels in the hippocampus, here we studied a potential role for hippocampal KORs in the renewal of extinguished fear. We found a dissociation in the contribution of hippocampal KORs, such that KORs in the VH, but not the DH, mediate the renewal of fear. The results from Experiment 1 showed that antagonizing KORs in the VH impaired the renewal of fear. Although recent research has clearly demonstrated a role for the VH in the return of fear following extinction, the DH has also been shown to mediate renewal. Furthermore, the DH in the rat projects to the dorsal region of the mPFC, and contains KORs. These experiments investigated the role of hippocampal KORs in the renewal of extinguished fear. We demonstrated that: 1) intra-VH microinfusions of the KOR antagonist norBNI significantly attenuated renewal using a within-subjects design, 2) both a 5 mg and 10 mg dose were equally effective at reducing CSfreezing in the training context, and 3) intra-DH microinfusions of norBNI had no effect on the expression of renewal. Together these experiments reveal a dissociation in hippocampal contributions to renewal, where KORs in the VH, but not the DH, contribute to the renewal of extinguished fear. These findings are consistent with previous studies demonstrating involvement of the hippocampus in fear renewal. However unlike previous studies, here we show a clear dissociation in the contribution of distinct hippocampal regions. Prior functional studies investigating the neural circuitry underlying renewal have used lesions or temporary inactivation methods to target either the DH or VH. Such studies found that inactivating either hippocampal region stabilizing reproductive division labor maintaining link physiological state foraging behavior prevented renewal. Clearly both the DH and VH are essential components of the circuitry mediating the return of fear following extinction, yet here we demonstrate that the contributions of these regions are distinct. Specifically, we demonstrated that only the VH involvement in renewal relies on activation of KORs, at least in part. Recently, Orsini end colleagues demonstrated that the VH mediates renewal via direct projections to the mPFC and BA. This raises the question of how KORs within the VH are acting on this circuit to mediate renewal. One possibility is through the extensive projections from the VH to the BA. Renewal increases Fos expression in BA-projecting neurons in the VH, and results in increased firing in a population of BA neurons receiving input from the VH. This suggests that recruitment of this VH-BA pathway is activated during renewal. Although activation of KORs in the hippocampus has been shown to inhibit excitatory transmission, in regions of the caudal hippocampus KORs are also located on GABAergic interneurons. As such, the attenuation of renewal seen here in Experiment 1 is potentially due to norBNI acting on these GABAergic interneurons to prevent the disinhibition of pyramidal neurons, reducing activation of the VHBA pathway and thus diminishing the response of fear neurons in the BA. Recently however, it was demonstrated that individual VH neurons send convergent projections to both the BA and mPFC, including the prelimbic cortex. This is of note considering the role of the PL in renewal and the expression of conditioned fear. For example, the PL shows significant neuronal activation during renewal, and CS-evoked firing which correlates with learned freezing behavior. Such findings raise the possibility that the attenuation of renewal by infusions of norBNI into the VH was due to simultaneous reduction in activity in both PL and BA. Of course it is important to note that KORs are widely distributed in the hippocampus, including on granule cell mossy fibres and perforant path terminals, and hence could exert numerous effects on hippocampal neurons.