The ability to associate the consumption of a taste with its positive or negative consequences is fundamental to survival and influences the behavior of species ranging from invertebrate to human. As a result, for both research and clinical reasons, there has been a great effort to understand the neuronal circuits, as well as the cellular and molecular mechanisms, underlying taste learning. From a neuroanatomical perspective, the contributions of the cortex and amygdala are well documented; however, the literature is riddled with conflicting results regarding the role of the hippocampus in different facets of taste learning. Here, we use conditional genetics in mice to block NMDA receptor-dependent plasticity individually in each of the three major hippocampal subfields, CA1, CA3, and the dentate gyrus, via deletion of the NR1 subunit. Across the CA1, CA3, and dentate gyrus NR1 knock-out lines, we uncover a pattern of differential deficits that establish the dispensability of hippocampal plasticity in incidental taste learning, the requirement of CA1 plasticity for associative taste learning, and a specific requirement for plasticity in the dentate gyrus when there is a long temporal gap between the taste and its outcome. Together, these data establish that the hippocampus is involved in associative taste learning and suggest an episodic component to this type of memory.