Contextual fear learning is a mental process, during which an originally neutral context becomes associated with a threat. Previous data have shown that one of the main controlling units of the defensive system, the central amygdala (CeA) is an active participant of contextual fear learning. Recently we showed that vasoactive intestinal polypeptide (VIP)-expressing neurons in the periaqueductal gray and dorsal raphe that innervate the CeA play a role in contextual fear acquisition, but not in the recall. As the primary source of contextual information is the hippocampus, we aimed to uncover the synaptic mechanisms underlying midbrain VIP neuron-driven changes at ventral hippocampal (vHC) fibers in the CeA. We hypothesized that VIP axon terminals from the midbrain would potentiate vHC inputs on CeA neurons thus inducing LTP. In line with this prediction, we found that in 60% of slices, LTP was successfully induced by stimulating the vHC and midbrain VIP axons subsequently. Furthermore, we compared the AMPA/NMDA current ratio at vHC afferents in CeA neurons between fear conditioned and control animals and found a significant increase after fear learning. However, reducing the activity of midbrain VIP neurons using chemogenetics could prevent the increase in the AMPA/NMDA ratio induced by fear learning. Our data thus show that the midbrain VIP inputs on CeA neurons is necessary for contextual fear learning by potentiating the vHC synapses by increasing the AMPA/NMDA ratio.