Krüger-Burg, Dilja D.

[["dc.bibliographiccitation.artnumber","151"],["dc.bibliographiccitation.journal","Frontiers in Behavioral Neuroscience"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Krueger-Burg, Dilja"],["dc.contributor.author","Winkler, Daniela"],["dc.contributor.author","Mitkovski, Miso"],["dc.contributor.author","Daher, Fernanda"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:34Z"],["dc.date.available","2017-09-07T11:46:34Z"],["dc.date.issued","2016"],["dc.description.abstract","Impairments in social skills are central to mental disease, and developing tools for their assessment in mouse models is essential. Here we present the SocioBox, a new behavioral paradigm to measure social recognition. Using this paradigm, we show that male wildtype mice of different strains can readily identify an unfamiliar mouse among 5 newly acquainted animals. In contrast, female mice exhibit lower locomotor activity during social exploration in the SocioBox compared to males and do not seem to discriminate between acquainted and unfamiliar mice, likely reflecting inherent differences in gender-specific territorial tasks. In addition to a simple quantification of social interaction time of mice grounded on predefined spatial zones (zone-based method), we developed a set of unbiased, data-driven analysis tools based on heat map representations and characterized by greater sensitivity. First proof-of-principle that the SocioBox allows diagnosis of social recognition deficits is provided using male PSD-95 heterozygous knockout mice, a mouse model related to psychiatric pathophysiology."],["dc.format.extent","12"],["dc.identifier.doi","10.3389/fnbeh.2016.00151"],["dc.identifier.gro","3150541"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13681"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7314"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The SocioBox: a novel paradigm to assess complex social recognition in male mice"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","41"],["dc.bibliographiccitation.journal","Behavioural Brain Research"],["dc.bibliographiccitation.lastpage","49"],["dc.bibliographiccitation.volume","251"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Winkler, Daniela"],["dc.contributor.author","Hammerschmidt, Kurt"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Krueger, Dilja"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Ritter, Caroline"],["dc.contributor.author","Jatho, Jasmin"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","Bourgeron, Thomas"],["dc.contributor.author","Fischer, Julia"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:47:38Z"],["dc.date.available","2017-09-07T11:47:38Z"],["dc.date.issued","2013"],["dc.description.abstract","Autism is the short name of a complex and heterogeneous group of disorders (autism spectrum disorders, ASD) with several lead symptoms required for classification, including compromised social interaction, reduced verbal communication and stereotyped repetitive behaviors/restricted interests. The etiology of ASD is still unknown in most cases but monogenic heritable forms exist that have provided insights into ASD pathogenesis and have led to the notion of autism as a 'synapse disorder'. Among the most frequent monogenic causes of autism are loss-of-function mutations of the NLGN4X gene which encodes the synaptic cell adhesion protein neuroligin-4X (NLGN4X). We previously described autism-like behaviors in male Nlgn4 null mutant mice, including reduced social interaction and ultrasonic communication. Here, we extend the phenotypical characterization of Nlgn4 null mutant mice to both genders and add a series of additional autism-relevant behavioral readouts. We now report similar social interaction and ultrasonic communication deficits in females as in males. Furthermore, aggression, nest-building parameters, as well as self-grooming and circling as indicators of repetitive behaviors/stereotypies were explored in both genders. The construction of a gender-specific autism severity composite score for Nlgn4 mutant mice markedly diminishes population/sample heterogeneity typically obtained for single tests, resulting in p values of <0.00001 and a genotype predictability of 100% for male and of >83% for female mice. Taken together, these data underscore the similarity of phenotypical consequences of Nlgn4/NLGN4X loss-of-function in mouse and man, and emphasize the high relevance of Nlgn4 null mutant mice as an ASD model with both construct and face validity."],["dc.identifier.doi","10.1016/j.bbr.2012.11.016"],["dc.identifier.gro","3142307"],["dc.identifier.isi","000322927700006"],["dc.identifier.pmid","23183221"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6831"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0166-4328"],["dc.subject","Social interaction; Nest building; Grooming; Repetitive behaviors; Stereotypies; Ultra-sound vocalization; Gender differences; ASD"],["dc.title","Development of an autism severity score for mice using Nlgn4 null mutants as a construct-valid model of heritable monogenic autism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1565"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","1579"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Kastner, Anne"],["dc.contributor.author","Poggi, Giulia"],["dc.contributor.author","Mitjans, Marina"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Hartmann, Annette M."],["dc.contributor.author","Van der Auwera, Sandra"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Krueger-Burg, Dilja"],["dc.contributor.author","Matuszko, Gabriela"],["dc.contributor.author","Brosi, Cornelia"],["dc.contributor.author","Homuth, Georg"],["dc.contributor.author","Völzke, H."],["dc.contributor.author","Benseler, Fritz"],["dc.contributor.author","Bagni, Claudia"],["dc.contributor.author","Fischer, Utz"],["dc.contributor.author","Dityatev, Alexander"],["dc.contributor.author","Grabe, Hans-Jörgen"],["dc.contributor.author","Rujescu, Dan"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:54:49Z"],["dc.date.available","2017-09-07T11:54:49Z"],["dc.date.issued","2015"],["dc.description.abstract","Fragile X syndrome (FXS) is mostly caused by a CGG triplet expansion in the fragile X mental retardation 1 gene (FMR1). Up to 60% of affected males fulfill criteria for autism spectrum disorder (ASD), making FXS the most frequent monogenetic cause of syndromic ASD. It is unknown, however, whether normal variants (independent of mutations) in the fragile X gene family (FMR1, FXR1, FXR2) and in FMR2 modulate autistic features. Here, we report an accumulation model of 8 SNPs in these genes, associated with autistic traits in a discovery sample of male patients with schizophrenia (N = 692) and three independent replicate samples: patients with schizophrenia (N = 626), patients with other psychiatric diagnoses (N = 111) and a general population sample (N = 2005). For first mechanistic insight, we contrasted microRNA expression in peripheral blood mononuclear cells of selected extreme group subjects with high-versus low-risk constellation regarding the accumulation model. Thereby, the brain-expressed miR-181 species emerged as potential \"umbrella regulator\", with several seed matches across the fragile X gene family and FMR2. To conclude, normal variation in these genes contributes to the continuum of autistic phenotypes."],["dc.identifier.doi","10.15252/emmm.201505696"],["dc.identifier.gro","3141771"],["dc.identifier.isi","000368135400005"],["dc.identifier.pmid","26612855"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12871"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/890"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1757-4684"],["dc.relation.issn","1757-4676"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Accumulated common variants in the broader fragile X gene family modulate autistic phenotypes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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","159"],["dc.bibliographiccitation.journal","Behavioural Brain Research"],["dc.bibliographiccitation.lastpage","164"],["dc.bibliographiccitation.volume","270"],["dc.contributor.author","Ju, Anes"],["dc.contributor.author","Hammerschmidt, Kurt"],["dc.contributor.author","Tantra, Martesa"],["dc.contributor.author","Krueger, Dilja"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:27Z"],["dc.date.available","2017-09-07T11:46:27Z"],["dc.date.issued","2014"],["dc.description.abstract","Neuroligin-4 (Nlgn4) is a member of the neuroligin family of postsynaptic cell adhesion molecules. Lossof-function mutations of NLGN4 are among the most frequent, known genetic causes of heritable autism.Adult Nlgn4 null mutant (Nlgn4−/−) mice are a construct valid model of human autism, with both gendersdisplaying a remarkable autistic phenotype, including deficits in social interaction and communication aswell as restricted and repetitive behaviors. In contrast to adults, autism-related abnormalities in neonataland juvenile Nlgn4−/− mice have not been reported yet. The present study has been designed tosystematically investigate in male and female Nlgn4−/− pups versus wildtype littermates (WT, Nlgn4+/+)developmental milestones and stimulus-induced ultrasound vocalization (USV). Neonatal development,followed daily from postnatal days (PND) 4 to 21, including physical development, neurological reflexesand neuromotor coordination, did not yield any differences between Nlgn4−/− and their WT littermates.USV in pups (PND8–9) in response to brief separation from their mothers revealed remarkable gendereffects, and a genotype influence in females regarding latency to first call. In juveniles (PND22–23),USV monitoring upon exposure to an anesthetized female intruder mouse uncovered a clear genotypeeffect with reduced USV in Nlgn4−/− mice, and again a more prominent phenotype in females. Together,these data support an early manifestation of communication deficits in Nlgn4−/− mice that appear morepronounced in immature females with their overall stronger USV as compared to males."],["dc.identifier.doi","10.1016/j.bbr.2014.05.019"],["dc.identifier.gro","3150517"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7290"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.subject","Neuroligin-4; C57BL/6J; Ultrasound or ultrasonic vocalization; Neonatal milestones; Neonatal development; Gender"],["dc.title","Juvenile manifestation of ultrasound communication deficits in the neuroligin-4 null mutant mouse model of autism"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["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.firstpage","516"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.lastpage","523"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Hammer, Matthieu"],["dc.contributor.author","Krueger-Burg, Dilja"],["dc.contributor.author","Tuffy, Liam Patrick"],["dc.contributor.author","Cooper, Benjamin Hillman"],["dc.contributor.author","Taschenberger, Holger"],["dc.contributor.author","Goswami, Sarit Pati"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Jonas, Peter"],["dc.contributor.author","Varoqueaux, Frederique"],["dc.contributor.author","Rhee, Jeong-Seop"],["dc.contributor.author","Brose, Nils"],["dc.date.accessioned","2017-09-07T11:46:34Z"],["dc.date.available","2017-09-07T11:46:34Z"],["dc.date.issued","2015"],["dc.description.abstract","Loss-of-function mutations in the synaptic adhesion protein Neuroligin-4 are among the most common genetic abnormalities associated with autism spectrum disorders, but little is known about the function of Neuroligin-4 and the consequences of its loss. We assessed synaptic and network characteristics in Neuroligin-4 knockout mice, focusing on the hippocampus as a model brain region with a critical role in cognition and memory, and found that Neuroligin-4 deletion causes subtle defects of the protein composition and function of GABAergic synapses in the hippocampal CA3 region. Interestingly, these subtle synaptic changes are accompanied by pronounced perturbations of γ-oscillatory network activity, which has been implicated in cognitive function and is altered in multiple psychiatric and neurodevelopmental disorders. Our data provide important insights into the mechanisms by which Neuroligin-4-dependent GABAergic synapses may contribute to autism phenotypes and indicate new strategies for therapeutic approaches."],["dc.identifier.doi","10.1016/j.celrep.2015.09.011"],["dc.identifier.gro","3150543"],["dc.identifier.pmid","26456829"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7316"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Perturbed Hippocampal Synaptic Inhibition and γ-Oscillations in a Neuroligin-4 Knockout Mouse Model of Autism"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]