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Recent studies demonstrate that functional disruption in resting-state networks contributes to cognitive and affective symptoms of bipolar disorder (BD), however, the functional connectivity (FC) pattern underlying BD II depression within the default mode network (DMN), salience network (SN), and frontoparietal network (FPN) is still not well understood. The primary aim of this study was to explore whether the pathophysiology of BD II derived from the pattern of FC within the DMN, SN, and FPN by using seed-based FC approach of resting-state functional magnetic resonance imaging (rs-fMRI).Ninety-six BD II patients and 100 HCs underwent rs-fMRI and three-dimensional structural data acquisition. All patients were either drug naive or unmedicated for at least 6 months. The following four regions of interest were used to conduct seed-based FC: the left posterior cingulate cortex (PCC) seed to probe the DMN, the left subgenual anterior cingulate cortex (sgACC) and amygdala seeds to probe the SN, the left dorsal lateral prefrontal cortex (dlPFC) seed to probe the FPN.Compared with HCs, patients with BD II demonstrated hypoconnectivity of the left PCC to the bilateral medial prefrontal cortex (mPFC) and bilateral precuneus/PCC, and of the left sgACC to the right inferior temporal gyrus (ITG); nevertheless, the left amygdala and dlPFC had no within-network hypo- or hyperconnectivity to any other SN and FPN regions.Our findings suggest that disrupted FC is located in the DMN and SN, especially in the PCC-mPFC and precuneus/PCC, and sgACC-ITG connectivity in BD II patients.This is the first study to demonstrate disrupted FC within the DMN and SN in BD II depression.We found decreased FC between the PCC and mPFC, precuneus/PCC within the DMN in patients with BD II.We found decreased FC between the sgACC and ITG within the SN in patients with BD II.