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

Andrew L. Eagle, Claire E. Manning, Elizabeth S. Williams, Ryan M. Bastle, Paula A. Gajewski, Amber Garrison, Alexis J. Wirtz, Seda Akguen, Katie Brandel-Ankrapp, Wilson Endege, Frederick M. Boyce, Yoshinori N. Ohnishi, Michelle Mazei-Robison, Ian Maze, Rachel L. Neve and Alfred J. Robison ()
Additional contact information
Andrew L. Eagle: Michigan State University
Claire E. Manning: Michigan State University
Elizabeth S. Williams: Michigan State University
Ryan M. Bastle: Icahn School of Medicine, Mount Sinai
Paula A. Gajewski: Michigan State University
Amber Garrison: Michigan State University
Alexis J. Wirtz: Michigan State University
Seda Akguen: Michigan State University
Katie Brandel-Ankrapp: Michigan State University
Wilson Endege: Massachusetts General Hospital
Frederick M. Boyce: Massachusetts General Hospital
Yoshinori N. Ohnishi: Kurume University School of Medicine
Michelle Mazei-Robison: Michigan State University
Ian Maze: Icahn School of Medicine, Mount Sinai
Rachel L. Neve: Massachusetts General Hospital
Alfred J. Robison: Michigan State University

Nature Communications, 2020, vol. 11, issue 1, 1-12

Abstract: Abstract 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.

Date: 2020
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DOI: 10.1038/s41467-020-17825-x

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