The amygdala modulates memory for changes in reward magnitude: involvement of the amygdaloid GABAergic system.

Rats with bilateral amygdala cannulae were trained to run a straight alley for a large or small food reward. Muscimol (MUS), a GABAA agonist, or bicuculline methiodide (BMI), a GABAA antagonist, were infused into the amygdala immediately after a reward shift. In Experiment 1, rats in the large-reward group were shifted to the small reward and immediately after received an infusion of vehicle or MUS bilaterally into the amygdala. The runway latencies of the shifted vehicle animals were increased in comparison with those of the unshifted controls. In contrast, the shifted MUS (0.0001 nM, but not 0.01 nM) animals displayed latencies that were comparable to those of unshifted animals by the second postshift day. These findings suggest that muscimol dose-dependently attenuated the memory of the reward reduction. In Experiment 2 rats were trained as before except they received bilateral infusions of BMI into the amygdala immediately after reward reduction. The shifted BMI (0.1 nM, but not 0.3 nM) animals displayed increased runway latencies, in comparison with those of shifted vehicle animals, by the second postshift day. These findings suggest that BMI dose-dependently enhanced memory of the reward reduction. In Experiment 3, animals were trained as before except they first experienced a reward increase before receiving post-training injections of vehicle, MUS (0.001 nM) or BMI (0.1 nM). On the next day the reward was reduced. Despite reward reduction, shifted BMI animals persisted displaying low latencies for more trials than did shifted MUS animals. These findings suggest that BMI enhanced memory for the reward increase. More generally, the findings suggest that the amygdala and its GABAergic system is involved in memory consolidation for both positive and negative affective experiences.