Anhedonia in Postpartum Depression: The Role of neuroinflammation and dopamine dysfunction

Anhedonia is a core symptom of postpartum depression, yet the underlying neurobiological mechanisms remain poorly understood. Emerging evidence suggests that postpartum biological adaptations, including sleep disruption, stress, hormonal fluctuations, and immune remodeling, may influence neural systems involved in motivation. In this review, we examine neuroinflammation as a potential contributor to maternal anhedonia through its effects on dopamine-dependent reward circuitry. We propose two complementary mechanisms by which inflammatory signaling may disrupt motivation: (1) local inflammatory effects within nucleus accumbens microcircuits regulating dopamine release; and (2) dysfunction of corticostriatal networks, whereby inflammation impairs prefrontal regulation and reward valuation processes, leading to downstream anhedonia. We further review neuroimaging evidence supporting reward-system abnormalities in postpartum depression and discuss how multimodal imaging approaches may help distinguish between proposed mechanistic models. Understanding these pathways may facilitate development of biologically informed interventions targeting maternal anhedonia.