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 a lley for a large or small food reward. Muscimol (MUS), a GABA(A) agoni st, or bicuculline methiodide (BMI), a GABA(A) antagonist, were infuse d into the amygdala immediately after a reward shift. In Experiment 1, rats in the large-reward group were shifted to the small reward and i mmediately after received an infusion of vehicle or MUS bilaterally in to the amygdala. The runway latencies of the shifted vehicle animals w ere increased in comparison with those of the unshifted controls. In c ontrast, the shifted MUS (0.001 nM, but not 0.01 nM) animals displayed latencies that were comparable to those of unshifted animals by the s econd postshift day. These findings suggest that muscimol dose-depende ntly attenuated the memory of the reward reduction. In Experiment 2 ra ts 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 latenc ies, in comparison with those of shifted vehicle animals, by the secon d postshift day. These findings suggest that BMI dose-dependently enha nced memory of the reward reduction. In Experiment 3, animals were tra ined 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 reduct ion, shifted BMI animals persisted displaying low latencies for more t rials than did shifted MUS animals. These findings suggest that BMI en hanced memory for the reward increase. More generally, the findings su ggest that the amygdala and its GABAergic system is involved in memory consolidation for both positive and negative affective experiences.