| dc.description.abstract | Research has shown that the nucleus accumbens (NAc) released less dopamine following unexpected reward loss. The current study further examined the function of the NAc in the initial and recovery processes of reward loss using the Reward Downshift (RD) task, a behavioral paradigm known to induce frustration in rats. Temporary neural manipulation of the NAc was hypothesized to leave the consummatory suppression accompanying RD postshift Stage 1 intact. However, during postshift Stage 2, NAc excitation and inhibition were predicted to facilitate and suppress recovery, respectively. To produce transient neural manipulation of the NAc, the study utilized a chemogenetic technique known as Designer Receptor Exclusively Activated by Designer Drugs (DREADDs), which involved an intracranial infusion of a viral construct to deliver the DREADD and an intraperitoneal injection of Clozapine N-Oxide (CNO), the activator drug for DREADD. DREADD activation prior to exposure to 32-to-2% sucrose downshift showed that NAc inhibition had no effects on consummatory behavior during both postshift stages. Similarly, NAc excitation did not disrupt the consummatory suppression typical of postshift Stage 1. However, during postshift Stage 2, NAc excitation produced a significantly lower level of sucrose consumption compared to controls. Our study was the first to explore NAc function using DREADDs in the RD situation, contributing to the current literature on the role of NAc in reward devaluation and recovery. | |
