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Background: The lateral septum (LS) is a critical social behavior node. The LS is activated by social novelty, and perturbing LS activity impairs social recognition. However, the neural circuits and cell signaling pathways that converge on the LS to mediate this behavior aren't known. We identify brain-derived neurotrophic factor (BDNF) in projection neurons from the basolateral amgydala (BLA) to the LS, and tropomyosin kinase B receptor (TrkB) signaling in LS neurons, as required for social novelty recognition. Methods: We used single-molecule fluorescent in-situ hybridization to quantify Ntrk2 expression in LS. Viral transgenesis was used to induce cre-recombinase mediated TrkB knockdown in LS to evaluate impact on social recognition behavior, and social novelty-induced c-Fos expression in the LS. We used viral approaches for projection-specific ablation and BDNF-depletion in BLA-LS projection neurons to assess the role of this circuit in social recognition behavior. Results: The majority of GABAergic neurons in LS express TrkB. TrkB knockdown in LS abolishes social novelty recognition, and decreases LS activation in response to social novelty. Selectively ablating BLA-LS projection neurons abolishes social novelty recognition behavior, an effect that is phenocopied by depleting BDNF in this circuit. Conclusions: BLA-LS projection neurons depend on BDNF expression to regulate social recognition in the mouse. Within the LS, neurons require intact TrkB receptor signaling to mediate this behavior.