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.firstpage","58"],["dc.bibliographiccitation.journal","Pharmacology Biochemistry and Behavior"],["dc.bibliographiccitation.lastpage","63"],["dc.bibliographiccitation.volume","111"],["dc.contributor.author","Zlomuzica, Armin"],["dc.contributor.author","Dere, Dorothea"],["dc.contributor.author","Dere, Ekrem"],["dc.date.accessioned","2018-11-07T09:18:59Z"],["dc.date.available","2018-11-07T09:18:59Z"],["dc.date.issued","2013"],["dc.description.abstract","The histaminergic system in the central nervous system is involved in a variety of physiological, pathological and behavioral processes. There is now substantial evidence for an important role of histaminergic neurotransmission in learning and memory related processes. The histamine H1 receptor (H1R) is the most abundant histamine receptor in the mammalian brain. We have recently demonstrated that the genetic inactivation of the H1R in mice impairs episodic-like memory, defined as the ability to remember previous experiences with respect to their content and their temporal and spatial context. The ability to encode and retrieve the temporal order of unique events, that is its temporal context, is a core feature of episodic memory. Here we asked whether episodic-like memory deficits of H1R-KO mice are possibly due to changes in the processing, encoding or maintenance of temporal or sequence information which is critical for episodic-like memory formation. H1R-KO mice were tested in the temporal object memory (TOM) task with different inter-trial intervals (ITIs). H1R-KO mice showed impaired TOM when being tested under both, short and longer Ills. Another aim of the study was to determine whether temporal order discrimination is based on either familiarity or recollection-based memory processes. The performance of wild type (WT) animals in the TOM task suggests that they used recollection-like discrimination strategies. (C) 2013 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.pbb.2013.08.008"],["dc.identifier.isi","000326991400009"],["dc.identifier.pmid","23981314"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28532"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0091-3057"],["dc.title","The histamine H1 receptor and recollection-based discrimination in a temporal order memory task in the mouse"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.contributor.author","Ambrozkiewicz, Mateusz C."],["dc.contributor.author","Borisova, Ekaterina"],["dc.contributor.author","Schwark, Manuela"],["dc.contributor.author","Ripamonti, Silvia"],["dc.contributor.author","Schaub, Theres"],["dc.contributor.author","Smorodchenko, Alina"],["dc.contributor.author","Weber, A. Ioana"],["dc.contributor.author","Rhee, Hong Jun"],["dc.contributor.author","Altas, Bekir"],["dc.contributor.author","Yilmaz, Rüstem"],["dc.contributor.author","Mueller, Susanne"],["dc.contributor.author","Piepkorn, Lars"],["dc.contributor.author","Horan, Stephen T."],["dc.contributor.author","Straussberg, Rachel"],["dc.contributor.author","Zaqout, Sami"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Rosário, Marta"],["dc.contributor.author","Boehm-Sturm, Philipp"],["dc.contributor.author","Borck, Guntram"],["dc.contributor.author","Willig, Katrin I."],["dc.contributor.author","Rhee, JeongSeop"],["dc.contributor.author","Tarabykin, Victor"],["dc.contributor.author","Kawabe, Hiroshi"],["dc.date.accessioned","2020-12-10T18:09:37Z"],["dc.date.available","2020-12-10T18:09:37Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41380-020-0714-8"],["dc.identifier.eissn","1476-5578"],["dc.identifier.issn","1359-4184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73708"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","The murine ortholog of Kaufman oculocerebrofacial syndrome protein Ube3b regulates synapse number by ubiquitinating Ppp3cc"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","421"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Reviews in the Neurosciences"],["dc.bibliographiccitation.lastpage","434"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Breeden, Prescott"],["dc.contributor.author","Dere, Dorothea"],["dc.contributor.author","Zlomuzica, Armin"],["dc.contributor.author","Dere, Ekrem"],["dc.date.accessioned","2018-11-07T10:13:47Z"],["dc.date.available","2018-11-07T10:13:47Z"],["dc.date.issued","2016"],["dc.description.abstract","Mental time travel (MTT) is the ability to remember past events and to anticipate or imagine events in the future. MTT globally serves to optimize decision-making processes, improve problem-solving capabilities and prepare for future needs. MTT is also essential in providing our concept of self, which includes knowledge of our personality, our strengths and weaknesses, as well as our preferences and aversions. We will give an overview in which ways the capacity of animals to perform MTT is different from humans. Based on the existing literature, we conclude that MTT might represent a quantitative rather than qualitative entity with a continuum of MTT capacities in both humans and nonhuman animals. Given its high complexity, MTT requires a large processing capacity in order to integrate multimodal stimuli during the reconstruction of past and/or future events. We suggest that these operations depend on a highly specialized working memory subsystem, 'the MTT platform', which might represent a necessary additional component in the multicomponent working memory model by Alan Baddeley."],["dc.identifier.doi","10.1515/revneuro-2015-0053"],["dc.identifier.isi","000376682900007"],["dc.identifier.pmid","26756089"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40500"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Walter De Gruyter Gmbh"],["dc.relation.issn","1607-8470"],["dc.relation.issn","0334-1763"],["dc.title","The mental time travel continuum: on the architecture, capacity, versatility and extension of the mental bridge into the past and future"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","135"],["dc.bibliographiccitation.journal","Neuropharmacology"],["dc.bibliographiccitation.lastpage","145"],["dc.bibliographiccitation.volume","106"],["dc.contributor.author","Zlomuzica, Armin"],["dc.contributor.author","Dere, Dorothea"],["dc.contributor.author","Binder, Sonja"],["dc.contributor.author","Silva, Maria Angelica De Souza"],["dc.contributor.author","Huston, Joseph P."],["dc.contributor.author","Dere, Ekrem"],["dc.date.accessioned","2018-11-07T10:12:18Z"],["dc.date.available","2018-11-07T10:12:18Z"],["dc.date.issued","2016"],["dc.description.abstract","Alzheimer's disease is a neurodegenerative disorder characterized by extracellular amyloid plaque deposits, mainly composed of amyloid-beta peptide and intracellular neurofibrillary tangles consisting of aggregated hyperphosphorylated tau protein. Amyloid-beta represents a neurotoxic proteolytic cleavage product of amyloid precursor protein. The progressive cognitive decline that is associated with Alzheimer's disease has been mainly attributed to a deficit in cholinergic neurotransmission due to the continuous degeneration of cholinergic neurons e.g. in the basal forebrain. There is evidence suggesting that other neurotransmitter systems including neuronal histamine also contribute to the development and maintenance of Alzheimer's disease-related cognitive deficits. Pathological changes in the neuronal histaminergic system of such patients are highly predictive of ensuing cognitive deficits. Furthermore, histamine-related drugs, including histamine 3 receptor antagonists, have been demonstrated to alleviate cognitive symptoms in Alzheimer's disease. This review summarizes findings from animal and clinical research on the relationship between the neuronal histaminergic system and cognitive deterioration in Alzheimer's disease. The significance of the neuronal histaminergic system as a promising target for the development of more effective drugs for the treatment of cognitive symptoms is discussed. Furthermore, the option to use histamine-related agents as neurogenesis-stimulating therapy that counteracts progressive brain atrophy in Alzheimer's disease is considered. This article is part of a Special Issue entitled 'Histamine Receptors'. (C) 2015 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neuropharm.2015.05.007"],["dc.identifier.isi","000378964500015"],["dc.identifier.pmid","26025658"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40210"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","1873-7064"],["dc.relation.issn","0028-3908"],["dc.title","Neuronal histamine and cognitive symptoms in Alzheimer's disease"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1180"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Stroke"],["dc.bibliographiccitation.lastpage","1186"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","Zerche, M."],["dc.contributor.author","Weißenborn, Karin"],["dc.contributor.author","Ott, C."],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Worthmann, Hans"],["dc.contributor.author","Hassouna, I."],["dc.contributor.author","Rentzsch, Katrin"],["dc.contributor.author","Tryc, A. B."],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Steiner, Johann"],["dc.contributor.author","Binder, Lutz"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Sirén, A.-L."],["dc.contributor.author","Stöcker, W."],["dc.contributor.author","Ehrenreich, Hanhelore"],["dc.date.accessioned","2017-09-07T11:44:23Z"],["dc.date.available","2017-09-07T11:44:23Z"],["dc.date.issued","2015"],["dc.description.abstract","Background and Purpose—Recently, we reported high seroprevalence (age-dependent up to >19%) of N-methyl-d-aspartate-receptor subunit NR1 (NMDAR1) autoantibodies in both healthy and neuropsychiatrically ill subjects (N=4236). Neuropsychiatric syndrome relevance was restricted to individuals with compromised blood–brain barrier, for example, apolipoprotein E4 (APOE4) carrier status, both clinically and experimentally. We now hypothesized that these autoantibodies may upon stroke be protective in individuals with hitherto intact blood–brain barrier, but harmful for subjects with chronically compromised blood–brain barrier.Methods—Of 464 patients admitted with acute ischemic stroke in the middle cerebral artery territory, blood for NMDAR1 autoantibody measurements and APOE4 carrier status as indicator of a preexisting leaky blood–brain barrier was collected within 3 to 5 hours after stroke. Evolution of lesion size (delta day 7–1) in diffusion-weighted magnetic resonance imaging was primary outcome parameter. In subgroups, NMDAR1 autoantibody measurements were repeated on days 2 and 7.Results—Of all 464 patients, 21.6% were NMDAR1 autoantibody–positive (immunoglobulin M, A, or G) and 21% were APOE4 carriers. Patients with magnetic resonance imaging data available on days 1 and 7 (N=384) were divided into 4 groups according to NMDAR1 autoantibody and APOE4 status. Groups were comparable in all stroke-relevant presenting characteristics. The autoantibody+/APOE4− group had a smaller mean delta lesion size compared with the autoantibody−/APOE4- group, suggesting a protective effect of circulating NMDAR1 autoantibodies. In contrast, the autoantibody+/APOE4+ group had the largest mean delta lesion area. NMDAR1 autoantibody serum titers dropped on day 2 and remounted by day 7.Conclusions—Dependent on blood–brain barrier integrity before an acute ischemic brain injury, preexisting NMDAR1 autoantibodies seem to be beneficial or detrimental."],["dc.identifier.doi","10.1161/strokeaha.114.008323"],["dc.identifier.gro","3151637"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8453"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0039-2499"],["dc.title","Preexisting Serum Autoantibodies Against the NMDAR Subunit NR1 Modulate Evolution of Lesion Size in Acute Ischemic Stroke"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2"],["dc.bibliographiccitation.journal","Behavioural Brain Research"],["dc.bibliographiccitation.lastpage","7"],["dc.bibliographiccitation.volume","352"],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Dere, Dorothea"],["dc.contributor.author","de Souza Silva, Maria Angelica"],["dc.contributor.author","Huston, Joseph P."],["dc.contributor.author","Zlomuzica, Armin"],["dc.date.accessioned","2020-12-10T14:22:34Z"],["dc.date.available","2020-12-10T14:22:34Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.bbr.2017.03.026"],["dc.identifier.issn","0166-4328"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71657"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Fellow travellers: Working memory and mental time travel in rodents"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","264"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The Cerebellum"],["dc.bibliographiccitation.lastpage","283"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Netrakanti, Pallavi Rao"],["dc.contributor.author","Cooper, Benjamin H."],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Poggi, Giulia"],["dc.contributor.author","Winkler, Daniela"],["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","2015"],["dc.description.abstract","Munc13-3 is a member of the Munc13 family of synaptic vesicle priming proteins and mainly expressed in cerebellar neurons. Munc13-3 null mutant (Munc13-3−/−) mice show decreased synaptic release probability at parallel fiber to Purkinje cell, granule cell to Golgi cell, and granule cell to basket cell synapses and exhibit a motor learning deficit at highest rotarod speeds. Since we detected Munc13-3 immunoreactivity in the dentate gyrus, as reported here for the first time, and current studies indicated a crucial role for the cerebellum in hippocampus-dependent spatial memory, we systematically investigated Munc13-3−/− mice versus wild-type littermates of both genders with respect to hippocampus-related cognition and a range of basic behaviors, including tests for anxiety, sensory functions, motor performance and balance, sensorimotor gating, social interaction and competence, and repetitive and compulsive behaviors. Neither basic behavior nor hippocampus-dependent cognitive performance, evaluated by Morris water maze, hole board working and reference memory, IntelliCage-based place learning including multiple reversals, and fear conditioning, showed any difference between genotypes. However, consistent with a disturbed cerebellar reflex circuitry, a reliable reduction in the acoustic startle response in both male and female Munc13-3−/− mice was found. To conclude, complete deletion of Munc13-3 leads to a robust decrease in the acoustic startle response. This readout of a fast cerebellar reflex circuitry obviously requires synaptic vesicle priming by Munc13-3 for full functionality, in contrast to other behavioral or cognitive features, where a nearly perfect compensation of Munc13-3 deficiency by related synaptic proteins has to be assumed."],["dc.identifier.doi","10.1007/s12311-015-0645-0"],["dc.identifier.gro","3150521"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7293"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.subject","Hippocampus; Immunohistochemistry; Acoustic startle response; IntelliCage; Spatial working and reference memory; Gender"],["dc.title","Fast Cerebellar Reflex Circuitry Requires Synaptic Vesicle Priming by Munc13-3"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","unknown"],["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"]]