(A) Impact of dopaminergic midbrain inputs onto intercalated cell (ITC) clusters, central amygdala (CeA), and basal amygdala (BLA). Dopaminergic inputs from ventral tegmental area/substantia nigra pars compacta (VTA/SNC) target amygdala ITC clusters and, to a lesser extent, BLA and CeA. The dorsomedial-intercalated cell (dm-ITC) cluster is more densely and differentially innervated than the ventromedial-intercalated cell (vm-ITC) cluster. Co-release of glutamate is mainly observed in CeA, whereas GABA co-release is prominent onto dm- and vm-ITCs. Released dopamine (DA) directly hyperpolarizes some dm-ITCs, and DA depresses inhibitory interactions between ITC clusters via presynaptic DRD1. Dopaminergic midbrain inputs can thus regulate the ITC network by inhibitory and disinhibitory mechanisms acting on different time scales. (B) Effects of early extinction on dopaminergic regulation of ITC cluster activity and interactions. Early extinction training enhances both direct fast inhibition of dm-ITCs, by biasing midbrain inputs toward GABA co-release, and disinhibition of vm-ITCs, by altering DA-mediated suppression of the dm-ITC→vm-ITC pathway. Together, this may tip the activity balance toward decreased dm-ITC and increased vm-ITC activity. We speculate that this could impact behavioral outcome by decreasing inhibition onto dm-ITC targets (such as CeL and extinction-promoting neurons in BLA), while promoting inhibition onto vm-ITC targets (such as fear-promoting neurons in centro-medial amygdala [CeM] and BLA).