Babaev, Olga

[["dc.bibliographiccitation.artnumber","5400"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Babaev, Olga"],["dc.contributor.author","Cruces-Solis, Hugo"],["dc.contributor.author","Piletti Chatain, Carolina"],["dc.contributor.author","Hammer, Matthieu"],["dc.contributor.author","Wenger, Sally"],["dc.contributor.author","Ali, Heba"],["dc.contributor.author","Karalis, Nikolaos"],["dc.contributor.author","de Hoz, Livia"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Yanagawa, Yuchio"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Taschenberger, Holger"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Krueger-Burg, Dilja"],["dc.date.accessioned","2019-07-09T11:50:16Z"],["dc.date.available","2019-07-09T11:50:16Z"],["dc.date.issued","2018"],["dc.description.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."],["dc.identifier.doi","10.1038/s41467-018-07762-1"],["dc.identifier.pmid","30573727"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15897"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59736"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/49"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/213342/EU//AIMS"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P10: Rekrutierung und Verankerung von Neurotransmitterrezeptoren an GABAergen Synapsen - Zellbiologie und molekulare Mechanismen"],["dc.relation.issn","2041-1723"],["dc.relation.workinggroup","RG Brose"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","612"],["dc.subject.mesh","Amygdala"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Anxiety Disorders"],["dc.subject.mesh","Cell Adhesion Molecules, Neuronal"],["dc.subject.mesh","Membrane Proteins"],["dc.subject.mesh","Mice"],["dc.subject.mesh","Mice, Knockout"],["dc.subject.mesh","Nerve Tissue Proteins"],["dc.subject.mesh","RNA Interference"],["dc.subject.mesh","Synapses"],["dc.subject.mesh","Synaptic Transmission"],["dc.title","IgSF9b regulates anxiety behaviors through effects on centromedial amygdala inhibitory synapses"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","56"],["dc.bibliographiccitation.journal","Neuropharmacology"],["dc.bibliographiccitation.lastpage","65"],["dc.bibliographiccitation.volume","100"],["dc.contributor.author","Babaev, Olga"],["dc.contributor.author","Botta, Paolo"],["dc.contributor.author","Meyer, Elisabeth"],["dc.contributor.author","Müller, Christian"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Lüthi, Andreas"],["dc.contributor.author","Krueger-Burg, Dilja"],["dc.date.accessioned","2017-09-07T11:46:15Z"],["dc.date.available","2017-09-07T11:46:15Z"],["dc.date.issued","2016"],["dc.description.abstract","Neuroligin 2 (Nlgn2) is a synaptic adhesion protein that plays a central role in the maturation and function of inhibitory synapses. Nlgn2 mutations have been associated with psychiatric disorders such as schizophrenia, and in mice, deletion of Nlgn2 results in a pronounced anxiety phenotype. To date, however, the molecular and cellular mechanisms linking Nlgn2 deletion to psychiatric phenotypes remain completely unknown. The aim of this study was therefore to define the role of Nlgn2 in anxiety-related neural circuits. To this end, we used a combination of behavioral, immunohistochemical, and electrophysiological approaches in Nlgn2 knockout (KO) mice to expand the behavioral characterization of these mice and to assess the functional consequences of Nlgn2 deletion in the amygdala. Moreover, we investigated the differential activation of anxiety-related circuits in Nlgn2 KO mice using a cFOS activation assay following exposure to an anxiogenic stimulus. We found that Nlgn2 is present at the majority of inhibitory synapses in the basal amygdala, where its deletion affects postsynaptic structures specifically at perisomatic sites and leads to impaired inhibitory synaptic transmission. Following exposure to an anxiogenic environment, Nlgn2 KO mice show a robust anxiety phenotype as well as exacerbated induction of cFOS expression specifically in CaMKII-positive projection neurons, but not in parvalbumin- or somatostatin-positive interneurons. Our data indicate that Nlgn2 deletion predominantly affects inhibitory synapses onto projection neurons in basal amygdala, resulting in decreased inhibitory drive onto these neurons and leading to their excessive activation under anxiogenic conditions. This article is part of the Special Issue entitled 'Synaptopathy--from Biology to Therapy'."],["dc.identifier.doi","10.1016/j.neuropharm.2015.06.016"],["dc.identifier.gro","3150464"],["dc.identifier.pmid","26142252"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7232"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Neuroligin 2 deletion alters inhibitory synapse function and anxiety-associated neuronal activation in the amygdala"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","The FASEB Journal"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Cruces‐Solis, Hugo"],["dc.contributor.author","Babaev, Olga"],["dc.contributor.author","Ali, Heba"],["dc.contributor.author","Piletti Chatain, Carolina"],["dc.contributor.author","Mykytiuk, Vasyl"],["dc.contributor.author","Balekoglu, Nursen"],["dc.contributor.author","Wenger, Sally"],["dc.contributor.author","Krueger-Burg, Dilja"],["dc.date.accessioned","2021-07-05T14:57:36Z"],["dc.date.available","2021-07-05T14:57:36Z"],["dc.date.issued","2021"],["dc.description.abstract","While the neural circuits mediating normal, adaptive defensive behaviors have been extensively studied, substantially less is currently known about the network mechanisms by which aberrant, pathological anxiety is encoded in the brain. Here we investigate in mice how deletion of Neuroligin-2 (Nlgn2), an inhibitory synapse-specific adhesion protein that has been associated with pathological anxiety and other psychiatric disorders, alters the communication between key brain regions involved in mediating defensive behaviors. To this end, we performed multi-site simultaneous local field potential (LFP) recordings from the basolateral amygdala (BLA), centromedial amygdala (CeM), bed nucleus of the stria terminalis (BNST), prefrontal cortex (mPFC) and ventral hippocampus (vHPC) in an open field paradigm. We found that LFP power in the vHPC was profoundly increased and was accompanied by an abnormal modulation of the synchrony of theta frequency oscillations particularly in the vHPC-mPFC-BLA circuit. Moreover, deletion of Nlgn2 increased beta and gamma frequency synchrony across the network, and this increase was associated with increased center avoidance. Local deletion of Nlgn2 in the vHPC and BLA revealed that they encode distinct aspects of this avoidance phenotype, with vHPC linked to immobility and BLA linked to a reduction in exploratory activity. Together, our data demonstrate that alterations in long-range functional connectivity link synaptic inhibition to abnormal defensive behaviors, and that both exaggerated activation of normal defensive circuits and recruitment of fundamentally distinct mechanisms contribute to this phenotype. Nlgn2 knockout mice therefore represent a highly relevant model to study the role of inhibitory synaptic transmission in the circuits underlying anxiety disorders."],["dc.identifier.doi","10.1096/fj.202002028RR"],["dc.identifier.pmid","33960026"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/87684"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/144"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-441"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P10: Rekrutierung und Verankerung von Neurotransmitterrezeptoren an GABAergen Synapsen - Zellbiologie und molekulare Mechanismen"],["dc.relation.eissn","1530-6860"],["dc.relation.issn","0892-6638"],["dc.relation.workinggroup","RG Brose"],["dc.rights","CC BY-NC 4.0"],["dc.title","Altered theta and beta oscillatory synchrony in a genetic mouse model of pathological anxiety"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]