Abstract
People with fetal alcohol spectrum disorders (FASD) are suffered from a wide range of interlinked cognitive and psychological problems. However, few therapeutic options are available for those patients due to limited dissection of its underlying etiology. Here we found that prenatal alcohol exposure (PAE) increases anxiety in mice due to a dysregulated functional connectivity between the anterior cingulate cortex (ACC) and basolateral amygdala (BLA). We also show that chemogenetic activation of excitatory neurons in the ACC reduced this anxiety behavior in the PAE mice. Interestingly, although the level of plasma corticosterone correlated with the increase in anxiety in the PAE, this level was not altered by chemogenetic activation of the ACC, suggesting that the functional connectivity between the ACC and the BLA does not alter the activity of the hypothalamic-pituitary-adrenal axis. Altogether, this study demonstrated that reduced excitation in the ACC is a cause of anxiety in the PAE mice, providing critical insights into the ACC-BLA neural circuit as a potential target for treating anxiety in FASD patients.