Role of the BLA-NAc pathway on recovery from frustrative nonreward

Unexpected reward downshifts induce transient suppression of consummatory behavior through a process involving frustrative nonreward. We hypothesized that the recovery of behavior rests on the extent to which the downshifted reward becomes an acceptable reward. We argued that this requires the basolateral amygdala (BLA) to switch from activating the central amygdala (CeA), which leads to suppression, to activating the nucleus accumbens (NAc), which enhances rewarding effects. This hypothesis was tested using Cre-dependent inhibitory and excitatory DREADDs expressed in BLA neurons projecting to the NAc. Rats were trained to consume 32% sucrose in preshift sessions and exposed to 2% sucrose in postshift sessions, generating transient consummatory suppression. Histology showed that an estimated 25-32% of BLA cells were involved in the projection to the NAc in each group. Virus controls treated with CNO were not different from vehicle-treated animals. Inhibition of the BLA-NAc pathway by the DREADD activator clozapine N-oxide (CNO) delayed recovery of normal licking behavior across postshift sessions relative to vehicle-treated animals. This effect was not attributable to locomotor interactions with licking. Excitation of the BLA-NAc pathway exhibited only a nonsignificant trend toward increased licking, but also a nonsignificant trend toward reduced activity in the conditioning box. These results provide support for the hypothesis that the BLA-NAc projection is involved in the recovery of consummatory behavior following violations of reward expectancies.