BackgroundPrenatal stress (PS) is a major risk factor for depression later in life, yet the cellular mechanisms linking early-life adversity to long-term affective vulnerability remain incompletely understood. Neuropeptide receptors have emerged as important modulators of stress-related psychopathology, but their roles in mitochondrial regulation within limbic circuits remain largely unexplored.MethodsA rat model of PS was established to assess depression-like behaviors in adulthood. Mitochondri
Disruption of a GalR2–mitochondrial axis in the ventral hippocampus contributes to depression-like phenotypes after prenatal stress
Zhi-Qing David Xu
