Dysregulations of the fear responses can lead to anxiety disorders such as post-traumatic stress disorder (PTSD). While exposure therapy (or extinction in rodents) can significantly reduce the fear-associated symptoms, its effectiveness is limited with fear recovering spontaneously over time. While the activation of the amygdala is central for normal fear-related behavior, its hyperactivation may be at the core of pathological conditions including PTSD. Previous (including ours) studies using the TetTag technology showed that a subset of basal amygdala (BA) neurons activated during contextual fear conditioning are reactivated during memory retrieval (we refer to them as fear neurons). Here we hypothesize that the inputs from BA fear neurons sparsely targeting distributed brain regions could represent potential targets for treating fear disorders. The BA comprises various neuronal cell types encoding positive or negative valence, which project preferentially to the nucleus accumbens (NAc) and the central amygdala, respectively. Intriguingly, the contribution of BA fear neurons projecting to the NAc to fear retrieval and extinction is unknown. Here, we employed the cfos-tTA TetTAg mouse technology combined with in situ hybridization, viral intersectional strategies and pharmaco/optogenetics to label, manipulate and monitor the BA neurons activated during contextual fear conditioning, as well as the BA fear neurons projecting to the NAc. Our data provide new insights into the role of amygdalar-accumbens pathway in processing aversive stimuli, and further, to better explain how extinction alters the original fear circuit.