Schlüter, Oliver M.

[["dc.bibliographiccitation.firstpage","228"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Biological Psychiatry"],["dc.bibliographiccitation.lastpage","235"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Mu, Ping"],["dc.contributor.author","Neumann, Peter A."],["dc.contributor.author","Panksepp, Jaak"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dong, Yan"],["dc.date.accessioned","2021-04-27T14:48:59Z"],["dc.date.available","2021-04-27T14:48:59Z"],["dc.date.issued","2011-02-01"],["dc.description.abstract","Dysregulation of excitatory synaptic input to nucleus accumbens (NAc) medium spiny neurons (MSNs) underlies a key pathophysiology of drug addiction and addiction-associated emotional and motivational alterations. Dynorphin peptides, which exhibit higher affinity to κ type opioid receptors, are upregulated within the NAc upon exposure to cocaine administration, and the increased dynorphin-signaling in the NAc has been critically implicated in negative mood observed in cocaine- or stress-exposed animals. Despite such apparent behavioral significance of the NAc dynorphins, the understanding of how dynorphins regulate excitatory synaptic transmission in the NAc remains incomplete."],["dc.identifier.doi","10.1016/j.biopsych.2010.09.014"],["dc.identifier.pmid","21030009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84507"],["dc.language.iso","en"],["dc.relation.eissn","1873-2402"],["dc.relation.issn","0006-3223"],["dc.title","Exposure to cocaine alters dynorphin-mediated regulation of excitatory synaptic transmission in nucleus accumbens neurons"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","35"],["dc.bibliographiccitation.journal","Behavioural Brain Research"],["dc.bibliographiccitation.lastpage","45"],["dc.bibliographiccitation.volume","352"],["dc.contributor.author","Winkler, Daniela"],["dc.contributor.author","Daher, Fernanda"],["dc.contributor.author","Wüstefeld, Liane"],["dc.contributor.author","Hammerschmidt, Kurt"],["dc.contributor.author","Poggi, Giulia"],["dc.contributor.author","Seelbach, Anna"],["dc.contributor.author","Krueger-Burg, Dilja"],["dc.contributor.author","Vafadari, Behnam"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Liu, Yanling"],["dc.contributor.author","Kaczmarek, Leszek"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Dere, Ekrem"],["dc.date.accessioned","2021-04-27T14:48:12Z"],["dc.date.available","2021-04-27T14:48:12Z"],["dc.date.issued","2018"],["dc.description.abstract","The postsynaptic density proteins 95 (PSD95) and 93 (PSD93) belong to a family of scaffolding proteins, the membrane-associated guanylate kinases (MAGUKs), which are highly enriched in synapses and responsible for organizing the numerous protein complexes required for synaptic development and plasticity. Genetic studies have associated MAGUKs with diseases like autism and schizophrenia, but knockout mice show severe, complex defects with difficult-to-interpret behavioral abnormalities due to major motor dysfunction which is atypical for psychiatric phenotypes. Therefore, rather than studying loss-of-function mutants, we comprehensively investigated the behavioral consequences of reduced PSD95 expression, using heterozygous PSD95 knockout mice (PSD95+/-). Specifically, we asked whether heterozygous PSD95 deficient mice would exhibit alterations in the processing of social stimuli and social behavior. Additionally, we investigated whether PSD95 and PSD93 would reveal any indication of functional or biological redundancy. Therefore, homozygous and heterozygous PSD93 deficient mice were examined in a similar behavioral battery as PSD95 mutants. We found robust hypersocial behavior in the dyadic interaction test in both PSD95+/- males and females. Additionally, male PSD95+/- mice exhibited higher levels of aggression and territoriality, while female PSD95+/- mice showed increased vocalization upon exposure to an anesthetized female mouse. Both male and female PSD95+/- mice revealed mild hypoactivity in the open field but no obvious motor deficit. Regarding PSD93 mutants, homozygous (but not heterozygous) knockout mice displayed prominent hypersocial behavior comparable to that observed in PSD95+/- mice, despite a more severe motor phenotype, which precluded several behavioral tests or their interpretation. Considering that PSD95 and PSD93 reduction provoke strikingly similar behavioral consequences, we explored a potential substitution effect and found increased PSD93 protein expression in hippocampal synaptic enrichment preparations of PSD95+/- mice. These data suggest that both PSD95 and PSD93 are involved in processing of social stimuli and control of social behavior. This important role may be partly assured by functional/behavioral and biological/biochemical redundancy."],["dc.identifier.doi","10.1016/j.bbr.2017.02.011"],["dc.identifier.pmid","28189758"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84497"],["dc.language.iso","en"],["dc.relation.eissn","1872-7549"],["dc.relation.issn","0166-4328"],["dc.title","Hypersocial behavior and biological redundancy in mice with reduced expression of PSD95 or PSD93"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","041014"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Physical Review X"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Abbott, B. P."],["dc.contributor.author","Abbott, R."],["dc.contributor.author","Abbott, T. D."],["dc.contributor.author","Abernathy, M. R."],["dc.contributor.author","Acernese, F."],["dc.contributor.author","Ackley, K."],["dc.contributor.author","Adams, C."],["dc.contributor.author","Adams, T."],["dc.contributor.author","Addesso, P."],["dc.contributor.author","Adhikari, R. X."],["dc.contributor.author","Chao, S."],["dc.contributor.author","Chen, Y."],["dc.contributor.author","Chung, S."],["dc.contributor.author","Dent, T."],["dc.contributor.author","Ghosh, S."],["dc.contributor.author","Gras, S."],["dc.contributor.author","Huang, S."],["dc.contributor.author","Karki, S."],["dc.contributor.author","Khan, S."],["dc.contributor.author","Munch, J."],["dc.contributor.author","Nguyen, T. T."],["dc.contributor.author","Oliver, M."],["dc.contributor.author","Qin, J."],["dc.contributor.author","Schmidt, J."],["dc.contributor.author","Singh, A."],["dc.contributor.author","Thomas, M."],["dc.contributor.author","Thomas, P."],["dc.contributor.author","Wang, H."],["dc.contributor.author","Wang, Y."],["dc.contributor.author","Westphal, T."],["dc.contributor.author","Zhang, M."],["dc.contributor.author","Zhang, Y."],["dc.contributor.author","Röver, C."],["dc.contributor.author","De, S."],["dc.date.accessioned","2016-11-04T09:18:28Z"],["dc.date.accessioned","2021-10-27T13:20:48Z"],["dc.date.available","2016-11-04T09:18:28Z"],["dc.date.available","2021-10-27T13:20:48Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1103/PhysRevX.6.041014"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13828"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91981"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.issn","2160-3308"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Improved analysis of GW150914 using a fully spin-precessing waveform model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","15504"],["dc.bibliographiccitation.issue","39"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","15517"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Krueger, Juliane M."],["dc.contributor.author","Favaro, Plinio D."],["dc.contributor.author","Liu, Mingna"],["dc.contributor.author","Kitlinska, Agata"],["dc.contributor.author","Huang, Xiaojie"],["dc.contributor.author","Raabe, Monika"],["dc.contributor.author","Akad, Derya S."],["dc.contributor.author","Liu, Yanling"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Xu, Weifeng"],["dc.contributor.author","Schlueter, Oliver M."],["dc.date.accessioned","2018-11-07T09:19:47Z"],["dc.date.available","2018-11-07T09:19:47Z"],["dc.date.issued","2013"],["dc.description.abstract","In the postsynaptic density of glutamatergic synapses, the discs large (DLG)-membrane-associated guanylate kinase (MAGUK) family of scaffolding proteins coordinates a multiplicity of signaling pathways to maintain and regulate synaptic transmission. Postsynaptic density-93 (PSD-93) is the most variable paralog in this family; it exists in six different N-terminal isoforms. Probably because of the structural and functional variability of these isoforms, the synaptic role of PSD-93 remains controversial. To accurately characterize the synaptic role of PSD-93, we quantified the expression of all six isoforms in the mouse hippocampus and examined them individually in hippocampal synapses. Using molecular manipulations, including overexpression, gene knockdown, PSD-93 knock-out mice combined with biochemical assays, and slice electrophysiology both in rat and mice, we demonstrate that PSD-93 is required at different developmental synaptic states to maintain the strength of excitatory synaptic transmission. This strength is differentially regulated by the six isoforms of PSD-93, including regulations of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor-active and inactive synapses, and activity-dependent modulations. Collectively, these results demonstrate that alternative combinations of N-terminal PSD-93 isoforms and DLG-MAGUK paralogs can fine-tune signaling scaffolds to adjust synaptic needs to regulate synaptic transmission."],["dc.identifier.doi","10.1523/JNEUROSCI.0019-12.2013"],["dc.identifier.isi","000324912500021"],["dc.identifier.pmid","24068818"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28724"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.title","Differential Roles of Postsynaptic Density-93 Isoforms in Regulating Synaptic Transmission"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Cellular Neuroscience"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Xu, Weifeng"],["dc.contributor.author","Löwel, Siegrid"],["dc.contributor.author","Schlüter, Oliver M."],["dc.date.accessioned","2021-04-14T08:23:50Z"],["dc.date.available","2021-04-14T08:23:50Z"],["dc.date.issued","2020"],["dc.description.abstract","Critical periods are postnatal, restricted time windows of heightened plasticity in cortical neural networks, during which experience refines principal neuron wiring configurations. Here, we propose a model with two distinct types of synapses, innate synapses that establish rudimentary networks with innate function, and gestalt synapses that govern the experience-dependent refinement process. Nascent gestalt synapses are constantly formed as AMPA receptor-silent synapses which are the substrates for critical period plasticity. Experience drives the unsilencing and stabilization of gestalt synapses, as well as synapse pruning. This maturation process changes synapse patterning and consequently the functional architecture of cortical excitatory networks. Ocular dominance plasticity (ODP) in the primary visual cortex (V1) is an established experimental model for cortical plasticity. While converging evidence indicates that the start of the critical period for ODP is marked by the maturation of local inhibitory circuits, recent results support our model that critical periods end through the progressive maturation of gestalt synapses. The cooperative yet opposing function of two postsynaptic signaling scaffolds of excitatory synapses, PSD-93 and PSD-95, governs the maturation of gestalt synapses. Without those proteins, networks do not progress far beyond their innate functionality, resulting in rather impaired perception. While cortical networks remain malleable throughout life, the cellular mechanisms and the scope of critical period and adult plasticity differ. Critical period ODP is initiated with the depression of deprived eye responses in V1, whereas adult ODP is characterized by an initial increase in non-deprived eye responses. Our model proposes the gestalt synapse-based mechanism for critical period ODP, and also predicts a different mechanism for adult ODP based on the sparsity of nascent gestalt synapses at that age. Under our model, early life experience shapes the boundaries (the gestalt) for network function, both for its optimal performance as well as for its pathological state. Thus, reintroducing nascent gestalt synapses as plasticity substrates into adults may improve the network gestalt to facilitate functional recovery."],["dc.identifier.doi","10.3389/fncel.2020.00213"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81065"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1662-5102"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Silent Synapse-Based Mechanisms of Critical Period Plasticity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S636"],["dc.bibliographiccitation.journal","European Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","S637"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Fred, S.M."],["dc.contributor.author","Casarotto, P."],["dc.contributor.author","Moliner, R."],["dc.contributor.author","Antila, H."],["dc.contributor.author","Schlüter, O."],["dc.contributor.author","Castrén, E."],["dc.date.accessioned","2022-03-01T11:45:08Z"],["dc.date.available","2022-03-01T11:45:08Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.euroneuro.2019.01.009"],["dc.identifier.pii","S0924977X19300094"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103225"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0924-977X"],["dc.title","P.1.06 TRKB receptor interaction with postsynaptic density proteins (PSD93 and PSD95) in the mechanism of antidepressants"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","451"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","The Neuroscientist"],["dc.bibliographiccitation.lastpage","459"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Huang, Yanhua H."],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dong, Yan"],["dc.date.accessioned","2021-04-27T14:48:29Z"],["dc.date.available","2021-04-27T14:48:29Z"],["dc.date.issued","2015-10"],["dc.description.abstract","A transient but prominent increase in the level of \"silent synapses\"--a signature of immature glutamatergic synapses that contain only NMDA receptors without stably expressed AMPA receptors--has been identified in the nucleus accumbens (NAc) following exposure to cocaine. As the NAc is a critical forebrain region implicated in forming addiction-associated behaviors, the initial discoveries have raised speculations about whether and how these drug-induced synapses mature and potentially contribute to addiction-related behaviors. Here, we summarize recent progress in recognizing the pathway-specific regulations of silent synapse maturation, and its diverse impacts on behavior. We provide an update of the guiding hypothesis--the \"neural rejuvenation hypothesis\"--with recently emerged evidence of silent synapses in cocaine craving and relapse."],["dc.identifier.doi","10.1177/1073858415579405"],["dc.identifier.pmid","25829364"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84501"],["dc.language.iso","en"],["dc.relation.eissn","1089-4098"],["dc.relation.issn","1073-8584"],["dc.title","Silent Synapses Speak Up: Updates of the Neural Rejuvenation Hypothesis of Drug Addiction"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e78883"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Sedej, Simon"],["dc.contributor.author","Klemen, Maša Skelin"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Rupnik, Marjan Slak"],["dc.date.accessioned","2019-07-09T11:54:37Z"],["dc.date.available","2019-07-09T11:54:37Z"],["dc.date.issued","2013-10-21"],["dc.description.abstract","Rab3a is a small GTPase of the Rab3 subfamily that acts during late stages of Ca2+-regulated exocytosis. Previous functional analysis in pituitary melanotrophs described Rab3a as a positive regulator of Ca2+-dependent exocytosis. However, the precise role of the Rab3a isoform on the kinetics and intracellular [Ca2+] sensitivity of regulated exocytosis, which may affect the availability of two major peptide hormones, α-melanocyte stimulating hormone (α- MSH) and β-endorphin in plasma, remain elusive. We employed Rab3a knock-out mice (Rab3a KO) to explore the secretory phenotype in melanotrophs from fresh pituitary tissue slices. High resolution capacitance measurements showed that Rab3a KO melanotrophs possessed impaired Ca2+-triggered secretory activity as compared to wild-type cells. The hampered secretion was associated with the absence of cAMP-guanine exchange factor II/ Epac2- dependent secretory component. This component has been attributed to high Ca2+-sensitive release-ready vesicles as determined by slow photo-release of caged Ca2+. Radioimmunoassay revealed that α-MSH, but not β-endorphin, was elevated in the plasma of Rab3a KO mice, indicating increased constitutive exocytosis of α-MSH. Increased constitutive secretion of α-MSH from incubated tissue slices was associated with reduced α-MSH cellular content in Rab3a-deficient pituitary cells. Viral re-expression of the Rab3a protein in vitro rescued the secretory phenotype of melanotrophs from Rab3a KO mice. In conclusion, we suggest that Rab3a deficiency promotes constitutive secretion and underlies selective impairment of Ca2+-dependent release of α-MSH."],["dc.format.extent","12"],["dc.identifier.doi","10.1371/journal.pone.0078883"],["dc.identifier.fs","599561"],["dc.identifier.pmid","24205339"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9423"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60693"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Rab3a Is Critical for Trapping Alpha-MSH Granules in the High Ca2+-Affinity Pool by Preventing Constitutive Exocytosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","985"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neuroscience"],["dc.bibliographiccitation.lastpage","1002"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Schlüter, O. M."],["dc.contributor.author","Fornai, F."],["dc.contributor.author","Alessandrí, M. G."],["dc.contributor.author","Takamori, S."],["dc.contributor.author","Geppert, M."],["dc.contributor.author","Jahn, R."],["dc.contributor.author","Südhof, T. C."],["dc.date.accessioned","2021-04-27T14:49:10Z"],["dc.date.available","2021-04-27T14:49:10Z"],["dc.date.issued","2003"],["dc.identifier.doi","10.1016/S0306-4522(03)00036-8"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84509"],["dc.relation.issn","0306-4522"],["dc.title","Role of α-synuclein in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced parkinsonism in mice"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["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"]]