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","1"],["dc.bibliographiccitation.journal","Cerebral Cortex"],["dc.bibliographiccitation.lastpage","14"],["dc.contributor.author","Unichenko, Petr"],["dc.contributor.author","Yang, Jenq-Wei"],["dc.contributor.author","Kirischuk, Sergei"],["dc.contributor.author","Kolbaev, Sergei"],["dc.contributor.author","Kilb, Werner"],["dc.contributor.author","Hammer, Matthieu"],["dc.contributor.author","Krueger-Burg, Dilja"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Luhmann, Heiko J."],["dc.date.accessioned","2018-03-08T09:21:32Z"],["dc.date.available","2018-03-08T09:21:32Z"],["dc.date.issued","2017"],["dc.description.abstract","Neuroligin-4 (Nlgn4) is a cell adhesion protein that regulates synapse organization and function. Mutations in human NLGN4 are among the causes of autism spectrum disorders. In mouse, Nlgn4 knockout (KO) perturbs GABAergic synaptic transmission and oscillatory activity in hippocampus, and causes social interaction deficits. The complex profile of cellular and circuit changes that are caused by Nlgn4-KO is still only partly understood. Using Nlgn4-KO mice, we found that Nlgn4-KO increases the power in the alpha frequency band of spontaneous network activity in the barrel cortex under urethane anesthesia in vivo. Nlgn4-KO did not affect single-whisker-induced local field potentials, but suppressed the late evoked multiunit activity in vivo. Although Nlgn4-KO did not affect evoked EPSCs in layer 4 (L4) spiny stellate cells in acute thalamocortical slices elicited by electrical stimulation of thalamocortical inputs, it caused a lower frequency of both miniature (m) IPSCs and mEPSCs, and a decrease in the number of readily releasable vesicles at GABAergic and glutamatergic connections, weakening both excitatory and inhibitory transmission. However, Nlgn4 deficit strongly suppresses glutamatergic activity, shifting the excitation–inhibition balance to inhibition. We conclude that Nlgn4-KO does not influence the incoming whisker-mediated sensory information to the barrel cortex, but modifies intracortical information processing."],["dc.identifier.doi","10.1093/cercor/bhx165"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/12907"],["dc.language.iso","en"],["dc.notes.intern","GRO-Li-Import"],["dc.notes.status","final"],["dc.relation.doi","10.1093/cercor/bhx165"],["dc.relation.issn","1047-3211"],["dc.relation.issn","1460-2199"],["dc.title","Autism Related Neuroligin-4 Knockout Impairs Intracortical Processing but not Sensory Inputs in Mouse Barrel Cortex"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["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.firstpage","408"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","410"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Krueger, Dilja D."],["dc.contributor.author","Brose, Nils"],["dc.date.accessioned","2017-09-07T11:47:42Z"],["dc.date.available","2017-09-07T11:47:42Z"],["dc.date.issued","2013"],["dc.description.abstract","In this issue of Neuron, Foldy et al. (2013) report that endocannabinoid-mediated signaling at inhibitory synapses is dysregulated in mouse models of autism-associated Neuroligin-3 mutations. These findings carry implications regarding the pathophysiology of autism spectrum disorders and the development of treatment strategies."],["dc.identifier.doi","10.1016/j.neuron.2013.04.030"],["dc.identifier.gro","3142351"],["dc.identifier.isi","000318961700002"],["dc.identifier.pmid","23664608"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7319"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Cell Press"],["dc.relation.issn","0896-6273"],["dc.title","Evidence for a Common Endocannabinoid-Related Pathomechanism in Autism Spectrum Disorders"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","S2211124721013590"],["dc.bibliographiccitation.firstpage","109889"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Berghoff, Stefan A."],["dc.contributor.author","Spieth, Lena"],["dc.contributor.author","Sun, Ting"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Depp, Constanze"],["dc.contributor.author","Sasmita, Andrew O."],["dc.contributor.author","Vasileva, Martina H."],["dc.contributor.author","Scholz, Patricia"],["dc.contributor.author","Zhao, Yu"],["dc.contributor.author","Krueger-Burg, Dilja"],["dc.contributor.author","Saher, Gesine"],["dc.date.accessioned","2021-12-01T09:23:54Z"],["dc.date.available","2021-12-01T09:23:54Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.celrep.2021.109889"],["dc.identifier.pii","S2211124721013590"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94788"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.issn","2211-1247"],["dc.title","Neuronal cholesterol synthesis is essential for repair of chronically demyelinated lesions in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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","451"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Genes, Brain and Behavior"],["dc.bibliographiccitation.lastpage","458"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Sidorov, M. S."],["dc.contributor.author","Krueger, D. D."],["dc.contributor.author","Taylor, M."],["dc.contributor.author","Gisin, E."],["dc.contributor.author","Osterweil, E. K."],["dc.contributor.author","Bear, M. F."],["dc.date.accessioned","2021-06-01T10:47:15Z"],["dc.date.available","2021-06-01T10:47:15Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1111/gbb.12137"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85534"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","1601-1848"],["dc.title","Extinction of an instrumental response: a cognitive behavioral assay in Fmr1 knockout mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","412"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Current Opinion in Neurobiology"],["dc.bibliographiccitation.lastpage","422"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Krueger, Dilja D."],["dc.contributor.author","Tuffy, Liam P."],["dc.contributor.author","Papadopoulos, Theofilos"],["dc.contributor.author","Brose, Nils"],["dc.date.accessioned","2017-09-07T11:48:51Z"],["dc.date.available","2017-09-07T11:48:51Z"],["dc.date.issued","2012"],["dc.description.abstract","Neurexins (NXs) and neuroligins (NLs) are transsynaptically interacting cell adhesion proteins that play a key role in the formation, maturation, activity-dependent validation, and maintenance of synapses. As complex alternative splicing processes in nerve cells generate a large number of NX and NLs variants, it has been proposed that a combinatorial interaction code generated by these variants may determine synapse identity and network connectivity during brain development. The functional importance of NXs and NLs is exemplified by the fact that mutations in NX and NL genes are associated with several neuropsychiatric disorders, most notably with autism. Accordingly, major research efforts have focused on the molecular mechanisms by which NXs and NLs operate at synapses. In this review, we summarize recent progress in this field and discuss emerging topics, such as the role of alternative interaction partners of NXs and NLs in synapse formation and function, and their relevance for synaptic plasticity in the mature brain. The novel findings highlight the fundamental importance of NX-NL interactions in a wide range of synaptic functions."],["dc.identifier.doi","10.1016/j.conb.2012.02.012"],["dc.identifier.gro","3142522"],["dc.identifier.isi","000306634700008"],["dc.identifier.pmid","22424845"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8882"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Current Biology Ltd"],["dc.relation.issn","0959-4388"],["dc.title","The role of neurexins and neuroligins in the formation, maturation, and function of vertebrate synapses"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["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"]]