A hyperdopaminergic state, such as stress, is associated with an increase in affective behavior. In this issue of Neuron, Marowsky and colleagues identify two clusters of paracapsular intercalated GABA neurons in amygdala slice preparations of GAD67-GFP mice. These GABA neurons mediate inhibition from cortical afferents to both the major input and output station of the amygdala, are inhibited during action of dopamine via D1 receptors, and are thus likely to represent important cellular players during dopaminergic disinhibition related to increased affective behavior.