Separate BNST Microcircuits Targeted by Direct Versus Amygdala-Relayed Prefrontal Inputs Mediate Dissociable
Hongxia Yuan1, Yongmei Zhong1, Xuehan Zhang1
1State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai 200032, China.
Cells
|January 28, 2026
Summary
Researchers found distinct brain circuits for anxiety, depression, and social deficits. The basolateral amygdala (BLA) relays signals from the prefrontal cortex (PFC) to the bed nucleus of the stria terminalis (BNST), dissociating emotional and social behaviors.
Area of Science:
- Neuroscience
- Behavioral Science
- Molecular Biology
Background:
- Anxiety, depression, and social impairment often co-occur clinically.
- The shared neural mechanisms underlying these conditions are not well understood.
Purpose of the Study:
- To investigate the neural circuitry connecting the prefrontal cortex (PFC) and the bed nucleus of the stria terminalis (BNST) in a mouse model.
- To determine how specific pathways within this circuit influence anxiety, depression, and social behaviors.
Main Methods:
- Utilized a mouse model of chronic social isolation.
- Employed circuit tracing and chemogenetic techniques to manipulate neural activity.
- Dissected distinct microcircuits within the BNST based on their input sources.
Main Results:
- Identified two key pathways: PFC → BLA → BNST (indirect) and PFC → BNST (direct).
- Inhibition of the indirect pathway (PFC → BLA → BNST) ameliorated anxiety, depression, and social deficits.
- Inhibition of the direct pathway (PFC → BNST) specifically improved social recognition, leaving emotional behaviors unaffected.
Conclusions:
- The basolateral amygdala (BLA) integrates PFC signals to modulate behavior broadly.
- Distinct BNST microcircuits dissociate affective and social behaviors.
- The indirect pathway influences affective symptoms, while the direct pathway governs social recognition, offering a model for clinical comorbidity.
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