Abstract
BACKGROUND: Recent work suggests that a history of chronic alcohol exposure can enhance the influence of nondrug reward cues on ongoing actions. This is often modeled in Pavlovian-to-instrumental transfer (PIT) tasks that examine the interaction between Pavlovian and instrumental learning processes, usually reflected as an increase in action vigor during the presentation of a reward-associated cue. Though prior chronic alcohol exposure strengthens this type of cue-guided behavior, the neural mechanisms underlying such enhancements are not known. METHODS: In the present work, we examined the contribution of the central amygdala (CeA), a region strongly implicated in PIT behaviors and functionally altered by chronic alcohol exposure. We utilized Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) to examine the impact of inhibitory and excitatory CeA manipulation on PIT behaviors in alcohol-naïve mice and mice with a history of chronic intermittent ethano vapor exposure and withdrawal (CIE). RESULTS: Replicating previous work, we found that a history of CIE strengthened baseline PIT, in the absence of any CeA manipulation. We also found that activation of both inhibitory and excitatory DREADDs expressed in CeA enhanced PIT in alcohol-naïve mice, though the latter markedly reduced response rates. However, in mice exposed to CIE, activation of excitatory DREADD receptors expressed in CeA appeared to weaken PIT. CONCLUSIONS: These results suggest that alcohol-induced disruptions in amygdala function may contribute to changes in appetitive behaviors, such as cue-guided responding, following chronic exposure to alcohol. Better elucidating the neural mechanisms that underlie disrupted cue-guided behavior following chronic alcohol exposure may help to understand and treat deficits in adaptive behavior associated with chronic alcohol use in humans.