To determine whether damage of the gustatory thalamus (the parvicellular region of the ventroposteromedial nucleus) disrupts the perceived value of reinforcing stimuli, the performance of rats with bilateral, electrophysiologically guided, electrolytic lesions of the area was examined in Experiment 1 with a progressive-ratio schedule of reinforcement. Lesioned rats showed normal concentration-dependent changes in break point (an index of the amount of effort a subject will expend to obtain reinforcement) and in consummatory responding (licking) for the sucrose reward. In the reward comparison procedure of Experiment 2, however, the same lesioned rats failed to show morphine-induced suppression of alanine consumption. The results provide no support for the view that the thalamic taste area is involved in the perception of the absolute reinforcing value of gustatory stimuli.

Neurologically intact rats expecting to receive a high-value reward (1.0 M sucrose), licked less for an unexpected low-value reward (0.15% saccharin) than did control subjects that only received the saccharin solution. This reward comparison effect, termed successive negative contrast, was eliminated after bilateral electrolytic lesions of the gustatory thalamus. The results are discussed in terms of disrupted memory processes that may have rendered the lesioned rats incapable of computing the relative reward value of the available solution (0.15% saccharin) with respect to the memory of the preferred solution (1.0 M sucrose).

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Using consummately contrast procedures and the same taste stimuli (0.15% saccharin and 1.0 M sucrose), the authors tested the hypothesis that lesions of the gustatory thalamus disrupt gustatory memory in 2 experiments. In Experiment 1, irrespective of the duration of the intersolution interval (0 s, 30 s, 1 min, 2 min, 4 min, 8 min), thalamic lesions had no influence on the expression of simultaneous contrast effects. In Experiment 2, thalamic lesions abolished anticipatory negative contrast at the 0-s intersolution interval. These results provide no support for the experimental hypothesis. Rather, the data seem best interpreted as a lesion-induced disruption of the comparison mechanism responsible for anticipatory negative contrast. By this analysis, different comparison mechanisms underlie simultaneous and anticipatory contrast effects.

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