ABSTRACT
The same monkeys with neurotoxic amygdala lesions that were tested by Málková et al. (1997) on visual discrimination learning for auditory secondary reinforcement were subsequently tested on a reinforcer devaluation task. In this procedure, monkeys learned a set of 60 object discrimination problems. Half of the positive (rewarded) objects were consistently rewarded with one particular foodstuff (Food-1), and the other half were rewarded with a different, approximately equally preferred foodstuff (Food-2). After acquiring the discrimination problems, monkeys were confronted with sessions of critical trials in which the rewarded objects were paired with each other, Food-1 objects with Food-2 objects. Before some of these critical test sessions, the monkey was allowed to eat its fill of one of the two foods in the home cage before beginning the test session. Hence, because the monkey was satiated on that reinforcer, its value was decreased. In the critical test sessions following satiation, monkeys tended to avoid objects baited with the devalued (satiated) reinforcer, compared to baseline sessions (that are not preceded by satiation). Neurotoxic amygdala lesions abolish this effect (Málková et al., 1997). This effect requires interaction between the amygdala and orbital prefrontal cortex: monkeys with crossed unilateral lesions of these structures, combined with forebrain commissurotomy, showed a similar abolition of reinforcer devaluation effects (Fig. 2; Baxter, Parker, Lindner, Izquierdo, & Murray, 2000).
