Dere, Ekrem

[["dc.bibliographiccitation.firstpage","136"],["dc.bibliographiccitation.journal","Neurobiology of Learning and Memory"],["dc.bibliographiccitation.lastpage","150"],["dc.bibliographiccitation.volume","150"],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Arinrad, Sahab"],["dc.contributor.author","Schmidt, Manuela"],["dc.contributor.author","Zeisberg, Elisabeth"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2020-12-10T15:20:34Z"],["dc.date.available","2020-12-10T15:20:34Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.nlm.2018.02.023"],["dc.identifier.issn","1074-7427"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72715"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Cognitive, emotional and social phenotyping of mice in an observer-independent setting"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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"]]

[["dc.bibliographiccitation.firstpage","4618"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","4635"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Tuoc, Tran"],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Nguyen, Huong"],["dc.contributor.author","Tonchev, Anton B."],["dc.contributor.author","Sun, Guoqiang"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Shi, Yanhong"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Stoykova, Anastassia"],["dc.date.accessioned","2017-09-07T11:46:21Z"],["dc.date.available","2017-09-07T11:46:21Z"],["dc.date.issued","2016"],["dc.description.abstract","The BAF chromatin remodeling complex plays an essential role in brain development. However its function in postnatal neurogenesis in hippocampus is still unknown. Here, we show that in postnatal dentate gyrus (DG), the BAF170 subunit of the complex is expressed in radial glial-like (RGL) progenitors and in cell types involved in subsequent steps of adult neurogenesis including mature astrocytes. Conditional deletion of BAF170 during cortical late neurogenesis as well as during adult brain neurogenesis depletes the pool of RGL cells in DG, and promotes terminal astrocyte differentiation. These derangements are accompanied by distinct behavioral deficits, as reflected by an impaired accuracy of place responding in the Morris water maze test, during both hidden platform as well as reversal learning. Inducible deletion of BAF170 in DG during adult brain neurogenesis resulted in mild spatial learning deficits, having a more pronounced effect on spatial learning during the reversal test. These findings demonstrate involvement of BAF170-dependent chromatin remodeling in hippocampal neurogenesis and cognition and suggest a specific role of adult neurogenesis in DG in adaptive behavior."],["dc.identifier.doi","10.1007/s12035-016-9948-5"],["dc.identifier.gro","3150498"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14191"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7269"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","0893-7648"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Ablation of BAF170 in developing and postnatal dentate gyrus affects neural stem cell proliferation, differentiation, and learning"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1489"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","1501"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Pan, Hong"],["dc.contributor.author","Oliveira, Bárbara"],["dc.contributor.author","Saher, Gesine"],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Tapken, Daniel"],["dc.contributor.author","Mitjans, Marina"],["dc.contributor.author","Seidel, Jan"],["dc.contributor.author","Wesolowski, Janina"],["dc.contributor.author","Wakhloo, Debia"],["dc.contributor.author","Klein-Schmidt, Christina"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Schwabe, Kerstin"],["dc.contributor.author","Trippe, Ralf"],["dc.contributor.author","Mätz-Rensing, Kerstin"],["dc.contributor.author","Berghoff, Stefan"],["dc.contributor.author","Al-Krinawe, Yazeed"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Mischke, Reinhard"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Krauss, Joachim K."],["dc.contributor.author","Hollmann, Michael"],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2020-12-10T18:09:36Z"],["dc.date.available","2020-12-10T18:09:36Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1038/s41380-017-0011-3"],["dc.identifier.eissn","1476-5578"],["dc.identifier.issn","1359-4184"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15575"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73703"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-SA 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-sa/4.0"],["dc.title","Uncoupling the widespread occurrence of anti-NMDAR1 autoantibodies from neuropsychiatric disease in a novel autoimmune model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","254"],["dc.bibliographiccitation.journal","Behavioural Brain Research"],["dc.bibliographiccitation.lastpage","263"],["dc.bibliographiccitation.volume","277"],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Winkler, Daniela"],["dc.contributor.author","Ritter, Caroline"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Poggi, Giulia"],["dc.contributor.author","Patzig, Julia"],["dc.contributor.author","Gernert, Manuela"],["dc.contributor.author","Müller, Christian"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Werner, Hauke B."],["dc.date.accessioned","2017-09-07T11:46:34Z"],["dc.date.available","2017-09-07T11:46:34Z"],["dc.date.issued","2015"],["dc.description.abstract","The neuronal tetraspan proteins, M6A (Gpm6a) and M6B (Gpm6b), belong to the family of proteolipids that are widely expressed in the brain. We recently reported Gpm6a deficiency as a monogenetic cause of claustrophobia in mice. Its homolog proteolipid, Gpm6b, is ubiquitously expressed in neurons and oligodendrocytes. Gpm6b is involved in neuronal differentiation and myelination. It interacts with the N-terminal domain of the serotonin transporter (SERT) and decreases cell-surface expression of SERT. In the present study, we employed Gpm6b null mutant mice (Gpm6b(-/-)) to search for behavioral functions of Gpm6b. We studied male and female Gpm6b(-/-) mice and their wild-type (WT, Gpm6b(+/+)) littermates in an extensive behavioral test battery. Additionally, we investigated whether Gpm6b(-/-) mice exhibit changes in the behavioral response to a 5-HT2A/C receptor agonist. We found that Gpm6b(-/-) mice display completely normal sensory and motor functions, cognition, as well as social and emotionality-like (anxiety, depression) behaviors. On top of this inconspicuous behavioral profile, Gpm6b(-/-) mice of both genders exhibit a selective impairment in prepulse inhibition of the acoustic startle response. Furthermore, in contrast to WT mice that show the typical locomotion suppression and increase in grooming activity after intraperitoneal administration of DOI [(±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride], Gpm6b(-/-) mice demonstrate a blunted behavioral response to this 5-HT2A/C receptor agonist. To conclude, Gpm6b deficiency impairs sensorimotor gating and modulates the behavioral response to a serotonergic challenge."],["dc.identifier.doi","10.1016/j.bbr.2014.04.021"],["dc.identifier.gro","3150542"],["dc.identifier.pmid","24768641"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7315"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.subject","Glycoprotein M6B; Prepulse inhibition; Serotonin transporter (SERT); Proteolipid protein (PLP); Gpm6a; C57BL/6J"],["dc.title","Gpm6b deficiency impairs sensorimotor gating and modulates the behavioral response to a 5-HT2A/C receptor agonist"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]