IgSF9b regulates anxiety behaviors through effects on centromedial amygdala inhibitory synapses
Autor: | Nils Brose, Holger Taschenberger, Olga Babaev, Carolina Piletti Chatain, Livia de Hoz, Sally Wenger, Heba Ali, Nikolaos Karalis, Yuchio Yanagawa, Oliver M. Schlüter, Dilja Krueger-Burg, Matthieu Hammer, Hugo Cruces-Solis, Hannelore Ehrenreich |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
medicine.drug_class Science Cell Adhesion Molecules Neuronal General Physics and Astronomy Nerve Tissue Proteins Biology Inhibitory postsynaptic potential Amygdala Anxiolytic Synaptic Transmission General Biochemistry Genetics and Molecular Biology Postsynapse Article Synapse 03 medical and health sciences Mice 0302 clinical medicine medicine Biological neural network IgSF9b Animals lcsh:Science Mice Knockout Multidisciplinary Membrane Proteins General Chemistry Anxiety Disorders 030104 developmental biology medicine.anatomical_structure Knockout mouse Synapses Anxiety lcsh:Q RNA Interference medicine.symptom Neuroscience 030217 neurology & neurosurgery |
Zdroj: | Nature Communications Nature Communications, Vol 9, Iss 1, Pp 1-16 (2018) |
ISSN: | 2041-1723 |
Popis: | 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. IgSF9b is a synaptic adhesion protein that has been linked to psychiatric disorders. Here the authors show that deletion of IgSF9b regulates anxiety-like behaviour in mice by increasing inhibitory synaptic transmission in the centromedial amygdala. |
Databáze: | OpenAIRE |
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