Abstract
Although most adults in the United States will drink alcohol in their life, only ∼6% will go on to develop an alcohol use disorder (AUD). While a great deal of work has furthered our understanding of the cycle of addiction, it remains unclear why certain people transition to disordered drinking. Altered activity in regions implicated in AUDs, like the basolateral amygdala (BLA), has been suggested to play a role in the pathophysiology of AUDs, but how these networks contribute to alcohol misuse remains unclear. Here we investigated how the impact of alcohol on the BLA network relates to alcohol exposure. We first examined the effect of acute ethanol administration on the BLA and frontal cortical networks and the relationship with subsequent voluntary ethanol consumption using the Intermittent Access paradigm. In addition, we recorded network activity from the BLA and frontal cortex throughout the Drinking-in-the-Dark-Multiple Scheduled Access paradigm to assess the impact of voluntary alcohol consumption on network states during binge and abstinence periods. Finally, we investigated the impact of acute withdrawal from chronic alcohol exposure on BLA and frontal cortex network states using the Chronic Intermittent Ethanol (vapor) paradigm. We demonstrate that across paradigms, ethanol alters low gamma band (40-70 Hz) oscillations and remarkably correlates with the extent of future voluntary ethanol consumption in the IA paradigm. These data suggest that BLA network states play a role in the mechanisms influencing voluntary alcohol intake.