Sensitivity to instrumental contingency degradation is mediated by the entorhinal cortex and its efferents via the dorsal hippocampus.

Previous studies have shown that electrolytic lesions of the dorsal hippocampus render the instrumental performance of rats insensitive to selective degradation of the action-outcome contingency (Corbit and Balleine, 2000). In the present experiments, we sought to replicate this finding and to examine the effects of excitotoxic lesions. In the first three experiments, rats with either electrolytic or NMDA lesions of the dorsal hippocampus and sham-lesioned controls were trained to press two levers, each of which delivered a unique food outcome, before their sensitivity to outcome devaluation and degradation of the instrumental contingency was assessed. Although we were able to replicate our original finding that electrolytic lesions of the dorsal hippocampus render rats insensitive to selective degradation of the instrumental contingency, NMDA lesions of the dorsal hippocampus had no effect. Neither lesion had any detectable effect on sensitivity to outcome devaluation. In experiment 4, we assessed the possibility that the effect of the electrolytic lesion resulted from damage to fibers originating in the retrohippocampal region (including both entorhinal cortex and subiculum) by examining the impact of bilateral NMDA-induced lesions of the retrohippocampus on the same tasks. Importantly, this lesion produced a deficit similar to that observed after electrolytic hippocampal lesions. The final experiment used a disconnection procedure to assess more directly whether damage to efferents from the retrohippocampal region, rather than the dorsal hippocampus itself, can account for the observed deficit. The data from these tests suggest that the deficits observed previously after electrolytic hippocampal lesions were the result of damage to entorhinal efferents.