IgSF9b regulates anxiety behaviors through effects on centromedial amygdala inhibitory synapses

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, Holger Taschenberger, Nils Brose and Dilja Krueger-Burg ()
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Olga Babaev: Max Planck Institute of Experimental Medicine
Hugo Cruces-Solis: Max Planck Institute of Experimental Medicine
Carolina Piletti Chatain: Max Planck Institute of Experimental Medicine
Matthieu Hammer: Max Planck Institute of Experimental Medicine
Sally Wenger: Max Planck Institute of Experimental Medicine
Heba Ali: Max Planck Institute of Experimental Medicine
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

Nature Communications, 2018, vol. 9, issue 1, 1-16

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-018-07762-1

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