Krüger-Burg, Dilja D.

[["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","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.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"]]

[["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","66"],["dc.bibliographiccitation.journal","Current Opinion in Neurobiology"],["dc.bibliographiccitation.lastpage","77"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Krueger-Burg, Dilja"],["dc.contributor.author","Papadopoulos, Theofilos"],["dc.contributor.author","Brose, Nils"],["dc.date.accessioned","2018-03-08T09:21:31Z"],["dc.date.available","2018-03-08T09:21:31Z"],["dc.date.issued","2017"],["dc.description.abstract","While the postsynaptic density of excitatory synapses is known to encompass a highly complex molecular machinery, the equivalent organizational structure of inhibitory synapses has long remained largely undefined. In recent years, however, substantial progress has been made towards identifying the full complement of organizational proteins present at inhibitory synapses, including submembranous scaffolds, intracellular signaling proteins, transsynaptic adhesion proteins, and secreted factors. Here, we summarize these findings and discuss future challenges in assigning synapse-specific functions to the newly discovered catalog of proteins, an endeavor that will depend heavily on newly developed technologies such as proximity biotinylation. Further advances are made all the more essential by growing evidence that links inhibitory synapses to psychiatric and neurological disorders."],["dc.identifier.doi","10.1016/j.conb.2017.04.003"],["dc.identifier.pmid","28460365"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/12904"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/10"],["dc.language.iso","en"],["dc.notes.intern","GRO-Li-Import"],["dc.notes.status","final"],["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.doi","10.1016/j.conb.2017.04.003"],["dc.relation.issn","0959-4388"],["dc.relation.issn","0959-4388"],["dc.relation.workinggroup","RG Brose"],["dc.title","Organizers of inhibitory synapses come of age"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","overview_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1037"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Psychopharmacology"],["dc.bibliographiccitation.lastpage","1062"],["dc.bibliographiccitation.volume","231"],["dc.contributor.author","Kleijer, Kristel T. E."],["dc.contributor.author","Schmeisser, Michael J."],["dc.contributor.author","Krueger, Dilja D."],["dc.contributor.author","Boeckers, Tobias M."],["dc.contributor.author","Scheiffele, Peter"],["dc.contributor.author","Bourgeron, Thomas"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Burbach, J. Peter H."],["dc.date.accessioned","2017-09-07T11:46:28Z"],["dc.date.available","2017-09-07T11:46:28Z"],["dc.date.issued","2014"],["dc.description.abstract","The genetic heterogeneity of autism spectrum disorders (ASDs) is enormous, and the neurobiology of proteins encoded by genes associated with ASD is very diverse. Revealing the mechanisms on which different neurobiological pathways in ASD pathogenesis converge may lead to the identification of drug targets. The main objective is firstly to outline the main molecular networks and neuronal mechanisms in which ASD gene products participate and secondly to answer the question how these converge. Finally, we aim to pinpoint drug targets within these mechanisms. Literature review of the neurobiological properties of ASD gene products with a special focus on the developmental consequences of genetic defects and the possibility to reverse these by genetic or pharmacological interventions. The regulation of activity-dependent protein synthesis appears central in the pathogenesis of ASD. Through sequential consequences for axodendritic function, neuronal disabilities arise expressed as behavioral abnormalities and autistic symptoms in ASD patients. Several known ASD gene products have their effect on this central process by affecting protein synthesis intrinsically, e.g., through enhancing the mammalian target of rapamycin (mTOR) signal transduction pathway or through impairing synaptic function in general. These are interrelated processes and can be targeted by compounds from various directions: inhibition of protein synthesis through Lovastatin, mTOR inhibition using rapamycin, or mGluR-related modulation of synaptic activity. ASD gene products may all feed into a central process of translational control that is important for adequate glutamatergic regulation of dendritic properties. This process can be modulated by available compounds but may also be targeted by yet unexplored routes."],["dc.identifier.doi","10.1007/s00213-013-3403-3"],["dc.identifier.gro","3142180"],["dc.identifier.isi","000332025500006"],["dc.identifier.pmid","24419271"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5421"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.eissn","1432-2072"],["dc.relation.issn","0033-3158"],["dc.title","Neurobiology of autism gene products: towards pathogenesis and drug targets"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]