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IgSF9b regulates anxiety behaviors through effects on centromedial amygdala inhibitory synapses

Author

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  • Olga Babaev

    (Max Planck Institute of Experimental Medicine
    Göttingen Graduate School for Neurosciences, Biophysics, and Molecular Biosciences)

  • Hugo Cruces-Solis

    (Max Planck Institute of Experimental Medicine)

  • Carolina Piletti Chatain

    (Max Planck Institute of Experimental Medicine
    Göttingen Graduate School for Neurosciences, Biophysics, and Molecular Biosciences)

  • Matthieu Hammer

    (Max Planck Institute of Experimental Medicine)

  • Sally Wenger

    (Max Planck Institute of Experimental Medicine)

  • Heba Ali

    (Max Planck Institute of Experimental Medicine
    Göttingen Graduate School for Neurosciences, Biophysics, and Molecular Biosciences)

  • Nikolaos Karalis

    (Friedrich Miescher Institute for Biomedical Research)

  • Livia de Hoz

    (Max Planck Institute of Experimental Medicine)

  • Oliver M. Schlüter

    (European Neuroscience Institute Göttingen)

  • Yuchio Yanagawa

    (Gunma University Graduate School of Medicine)

  • Hannelore Ehrenreich

    (Max Planck Institute of Experimental Medicine)

  • Holger Taschenberger

    (Max Planck Institute of Experimental Medicine)

  • Nils Brose

    (Max Planck Institute of Experimental Medicine)

  • Dilja Krueger-Burg

    (Max Planck Institute of Experimental Medicine)

Abstract

Abnormalities in synaptic inhibition play a critical role in psychiatric disorders, and accordingly, it is essential to understand the molecular mechanisms linking components of the inhibitory postsynapse to psychiatrically relevant neural circuits and behaviors. Here we study the role of IgSF9b, an adhesion protein that has been associated with affective disorders, in the amygdala anxiety circuitry. We show that deletion of IgSF9b normalizes anxiety-related behaviors and neural processing in mice lacking the synapse organizer Neuroligin-2 (Nlgn2), which was proposed to complex with IgSF9b. This normalization occurs through differential effects of Nlgn2 and IgSF9b at inhibitory synapses in the basal and centromedial amygdala (CeM), respectively. Moreover, deletion of IgSF9b in the CeM of adult Nlgn2 knockout mice has a prominent anxiolytic effect. Our data place IgSF9b as a key regulator of inhibition in the amygdala and indicate that IgSF9b-expressing synapses in the CeM may represent a target for anxiolytic therapies.

Suggested Citation

  • Olga Babaev & Hugo Cruces-Solis & Carolina Piletti Chatain & Matthieu Hammer & Sally Wenger & Heba Ali & Nikolaos Karalis & Livia de Hoz & Oliver M. Schlüter & Yuchio Yanagawa & Hannelore Ehrenreich &, 2018. "IgSF9b regulates anxiety behaviors through effects on centromedial amygdala inhibitory synapses," Nature Communications, Nature, vol. 9(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-07762-1
    DOI: 10.1038/s41467-018-07762-1
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