Diagenode

Circuit-specific hippocampal ΔFosB underlies resilience to stress-induced social avoidance.


Eagle, Andrew L and Manning, Claire E and Williams, Elizabeth S and Bastle, Ryan M and Gajewski, Paula A and Garrison, Amber and Wirtz, Alexis J and Akguen, Seda and Brandel-Ankrapp, Katie and Endege, Wilson and Boyce, Frederick M and Ohnishi, Yoshinori N

Chronic stress is a key risk factor for mood disorders like depression, but the stress-induced changes in brain circuit function and gene expression underlying depression symptoms are not completely understood, hindering development of novel treatments. Because of its projections to brain regions regulating reward and anxiety, the ventral hippocampus is uniquely poised to translate the experience of stress into altered brain function and pathological mood, though the cellular and molecular mechanisms of this process are not fully understood. Here, we use a novel method of circuit-specific gene editing to show that the transcription factor ΔFosB drives projection-specific activity of ventral hippocampus glutamatergic neurons causing behaviorally diverse responses to stress. We establish molecular, cellular, and circuit-level mechanisms for depression- and anxiety-like behavior in response to stress and use circuit-specific gene expression profiling to uncover novel downstream targets as potential sites of therapeutic intervention in depression.

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Published
September, 2020

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Products used in this publication

  • CRISPR/Cas9 Antibody
    C15200229-100
    CRISPR/Cas9 monoclonal antibody

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