Rats reduce intake of a palatable saccharin solution when followed by access to a preferred sucrose solution. This phenomenon, referred to as an anticipatory contrast effect (ACE), is thought to occur because the value of the saccharin conditioned stimulus (CS) pales in comparison to the highly rewarding sucrose unconditioned stimulus (US) expected in the near future. Although relatively little is known about the underlying neural substrates, lesions of the gustatory thalamus (THLX) fully disrupt the phenomenon (38, 40). The present set of experiments revisited this issue to determine the nature of this deficit. Rats with bilateral ibotenic acid lesions of the gustatory thalamus were given 3 min access to 0.15% saccharin and, after a zero sec or 5 min interval, were given 3 min access to either the same saccharin solution or a highly preferred 1.0 M sucrose solution. In Experiment 1, ACE testing began with the 5 min interstimulus interval (ISI) and then switched to the zero sec ISI. For Experiment 2, the order of ISI testing was reversed. The results show that axon-sparing, neurotoxic lesions of the gustatory thalamus prevent ACEs when using a zero second ISI and lead to a reversal (i.e., a reinforcement effect) when using a 5 min ISI. Taken together, the results suggest that the lesion leads to a specific reward comparison deficit whereby the rats fail to compare the value of an available reward with the memory of a preferred reward that is anticipated in the near future.