Göbbels, Sandra

[["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.contributor.author","Butt, Umer Javed"],["dc.contributor.author","Steixner-Kumar, Agnes A."],["dc.contributor.author","Depp, Constanze"],["dc.contributor.author","Sun, Ting"],["dc.contributor.author","Hassouna, Imam"],["dc.contributor.author","Wüstefeld, Liane"],["dc.contributor.author","Arinrad, Sahab"],["dc.contributor.author","Zillmann, Matthias R."],["dc.contributor.author","Schopf, Nadine"],["dc.contributor.author","Fernandez Garcia-Agudo, Laura"],["dc.contributor.author","Mohrmann, Leonie"],["dc.contributor.author","Bode, Ulli"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Hindermann, Martin"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Katschinski, Dörthe M."],["dc.contributor.author","Miskowiak, Kamilla W."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2021-04-14T08:28:40Z"],["dc.date.available","2021-04-14T08:28:40Z"],["dc.date.issued","2021"],["dc.description.abstract","Physical activity and cognitive challenge are established non-invasive methods to induce comprehensive brain activation and thereby improve global brain function including mood and emotional well-being in healthy subjects and in patients. However, the mechanisms underlying this experimental and clinical observation and broadly exploited therapeutic tool are still widely obscure. Here we show in the behaving brain that physiological (endogenous) hypoxia is likely a respective lead mechanism, regulating hippocampal plasticity via adaptive gene expression. A refined transgenic approach in mice, utilizing the oxygen-dependent degradation (ODD) domain of HIF-1α fused to CreERT2 recombinase, allows us to demonstrate hypoxic cells in the performing brain under normoxia and motor-cognitive challenge, and spatially map them by light-sheet microscopy, all in comparison to inspiratory hypoxia as strong positive control. We report that a complex motor-cognitive challenge causes hypoxia across essentially all brain areas, with hypoxic neurons particularly abundant in the hippocampus. These data suggest an intriguing model of neuroplasticity, in which a specific task-associated neuronal activity triggers mild hypoxia as a local neuron-specific as well as a brain-wide response, comprising indirectly activated neurons and non-neuronal cells."],["dc.identifier.doi","10.1038/s41380-020-00988-w"],["dc.identifier.pmid","33564132"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82678"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/31"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/104"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | C01: Oligodendroglial NMDA receptors and NMDAR1 autoantibodies as determinants of axonal integrity in neuropsychiatric disease"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | Z02: Integrative Datenanalyse und -interpretation. Generierung einer synaptisch-integrativen Datenstrategie (SynIDs)"],["dc.relation.eissn","1476-5578"],["dc.relation.issn","1359-4184"],["dc.relation.workinggroup","RG Ehrenreich (Clinical Neuroscience)"],["dc.relation.workinggroup","RG Nave (Neurogenetics)"],["dc.relation.workinggroup","RG Bonn"],["dc.rights","CC BY 4.0"],["dc.title","Hippocampal neurons respond to brain activity with functional hypoxia"],["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","486"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","499"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Oltrogge, Jan H."],["dc.contributor.author","Wolfer, Susanne"],["dc.contributor.author","Wieser, Georg L."],["dc.contributor.author","Nientiedt, Tobias"],["dc.contributor.author","Pieper, Alexander"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Groszer, Matthias"],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2018-11-07T09:09:46Z"],["dc.date.available","2018-11-07T09:09:46Z"],["dc.date.issued","2012"],["dc.description.abstract","Tomacula and myelin outfoldings are striking neuropathological features of a diverse group of inherited demyelinating neuropathies. Whereas the underlying genetic defects are well known, the molecular mechanisms of tomacula formation have remained obscure. We hypothesized that they are caused by uncontrolled, excessive myelin membrane growth, a process, which is regulated in normal development by neuregulin-1/ErbB2, PI3 Kinase signalling and ERK/MAPK signalling. Here, we demonstrate by targeted disruption of Pten in Schwann cells that hyperactivation of the endogenous PI3 Kinase pathway causes focal hypermyelination, myelin outfoldings and tomacula, even when induced in adult animals by tamoxifen, and is associated with progressive peripheral neuropathy. Activated AKT kinase is associated with PtdIns(3,4,5)P3 at paranodal loops and SchmidtLanterman incisures. This striking myelin pathology, with features of human CMT type 4B1 and HNPP, is dependent on AKT/mTOR signalling, as evidenced by a significant amelioration of the pathology in mice treated with rapamycin. We suggest that regions of non-compact myelin are under lifelong protection by PTEN against abnormal membrane outgrowth, and that dysregulated phosphoinositide levels play a critical role in the pathology of tomaculous neuropathies."],["dc.identifier.doi","10.1002/emmm.201200227"],["dc.identifier.isi","000304767900007"],["dc.identifier.pmid","22488882"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7777"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26338"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1757-4676"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Genetic disruption of Pten in a novel mouse model of tomaculous neuropathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","528"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","539"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Hagemeyer, Nora"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Hofer, Sabine"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Gerwig, Ulrike C."],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Wieser, Georg L."],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Gurvich, Artem"],["dc.contributor.author","Heckers, Stephan H."],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-08-25T10:14:17Z"],["dc.date.available","2017-08-25T10:14:17Z"],["dc.date.issued","2012"],["dc.description.abstract","Severe mental illnesses have been linked to white matter abnormalities, documented by postmortem studies. However, cause and effect have remained difficult to distinguish. CNP (2',3'-cyclic nucleotide 3'-phosphodiesterase) is among the oligodendrocyte/myelin-associated genes most robustly reduced on mRNA and protein level in brains of schizophrenic, bipolar or major depressive patients. This suggests that CNP reduction might be critical for a more general disease process and not restricted to a single diagnostic category. We show here that reduced expression of CNP is the primary cause of a distinct behavioural phenotype, seen only upon aging as an additional 'pro-inflammatory hit'. This phenotype is strikingly similar in Cnp heterozygous mice and patients with mental disease carrying the AA genotype at CNP SNP rs2070106. The characteristic features in both species with their partial CNP 'loss-of-function' genotype are best described as 'catatonia-depression' syndrome. As a consequence of perturbed CNP expression, mice show secondary low-grade inflammation/neurodegeneration. Analogously, in man, diffusion tensor imaging points to axonal loss in the frontal corpus callosum. To conclude, subtle white matter abnormalities inducing neurodegenerative changes can cause/amplify psychiatric diseases."],["dc.identifier.doi","10.1002/emmm.201200230"],["dc.identifier.gro","3150560"],["dc.identifier.pmid","22473874"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7776"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7334"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A myelin gene causative of a catatonia-depression syndrome upon aging"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6125"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","6148"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Runge, Karen"],["dc.contributor.author","Mathieu, Rémi"],["dc.contributor.author","Bugeon, Stéphane"],["dc.contributor.author","Lafi, Sahra"],["dc.contributor.author","Beurrier, Corinne"],["dc.contributor.author","Sahu, Surajit"],["dc.contributor.author","Schaller, Fabienne"],["dc.contributor.author","Loubat, Arthur"],["dc.contributor.author","Herault, Leonard"],["dc.contributor.author","Gaillard, Stéphane"],["dc.contributor.author","Pallesi-Pocachard, Emilie"],["dc.contributor.author","Montheil, Aurélie"],["dc.contributor.author","Bosio, Andreas"],["dc.contributor.author","Rosenfeld, Jill A"],["dc.contributor.author","Hudson, Eva"],["dc.contributor.author","Lindstrom, Kristin"],["dc.contributor.author","Mercimek-Andrews, Saadet"],["dc.contributor.author","Jeffries, Lauren"],["dc.contributor.author","van Haeringen, Arie"],["dc.contributor.author","Vanakker, Olivier"],["dc.contributor.author","Van Hecke, Audrey"],["dc.contributor.author","Amrom, Dina"],["dc.contributor.author","Küry, Sebastien"],["dc.contributor.author","Ratner, Chana"],["dc.contributor.author","Jethva, Reena"],["dc.contributor.author","Gamble, Candace"],["dc.contributor.author","Jacq, Bernard"],["dc.contributor.author","Fasano, Laurent"],["dc.contributor.author","Santpere, Gabriel"],["dc.contributor.author","Lorente-Galdos, Belen"],["dc.contributor.author","Sestan, Nenad"],["dc.contributor.author","Gelot, Antoinette"],["dc.contributor.author","Giacuzz, Sylvie"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Represa, Alfonso"],["dc.contributor.author","Cardoso, Carlos"],["dc.contributor.author","Cremer, Harold"],["dc.contributor.author","de Chevigny, Antoine"],["dc.date.accessioned","2022-08-09T12:22:40Z"],["dc.date.available","2022-08-09T12:22:40Z"],["dc.date.issued","2021"],["dc.description.abstract","While the transcription factor NEUROD2 has recently been associated with epilepsy, its precise role during nervous system development remains unclear. Using a multi-scale approach, we set out to understand how Neurod2 deletion affects the development of the cerebral cortex in mice. In Neurod2 KO embryos, cortical projection neurons over-migrated, thereby altering the final size and position of layers. In juvenile and adults, spine density and turnover were dysregulated in apical but not basal compartments in layer 5 neurons. Patch-clamp recordings in layer 5 neurons of juvenile mice revealed increased intrinsic excitability. Bulk RNA sequencing showed dysregulated expression of many genes associated with neuronal excitability and synaptic function, whose human orthologs were strongly associated with autism spectrum disorders (ASD). At the behavior level, Neurod2 KO mice displayed social interaction deficits, stereotypies, hyperactivity, and occasionally spontaneous seizures. Mice heterozygous for Neurod2 had similar defects, indicating that Neurod2 is haploinsufficient. Finally, specific deletion of Neurod2 in forebrain excitatory neurons recapitulated cellular and behavioral phenotypes found in constitutive KO mice, revealing the region-specific contribution of dysfunctional Neurod2 in symptoms. Informed by these neurobehavioral features in mouse mutants, we identified eleven patients from eight families with a neurodevelopmental disorder including intellectual disability and ASD associated with NEUROD2 pathogenic mutations. Our findings demonstrate crucial roles for Neurod2 in neocortical development, whose alterations can cause neurodevelopmental disorders including intellectual disability and ASD."],["dc.identifier.doi","10.1038/s41380-021-01179-x"],["dc.identifier.pmid","34188164"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112704"],["dc.language.iso","en"],["dc.relation.eissn","1476-5578"],["dc.relation.haserratum","/handle/2/88325"],["dc.relation.issn","1359-4184"],["dc.relation.issn","1476-5578"],["dc.rights","CC BY 4.0"],["dc.title","Disruption of NEUROD2 causes a neurodevelopmental syndrome with autistic features via cell-autonomous defects in forebrain glutamatergic neurons"],["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","1752"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","1767"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Hassouna, I."],["dc.contributor.author","Ott, C."],["dc.contributor.author","Wüstefeld, L."],["dc.contributor.author","Offen, N."],["dc.contributor.author","Neher, R. A."],["dc.contributor.author","Mitkovski, M."],["dc.contributor.author","Winkler, D."],["dc.contributor.author","Sperling, S."],["dc.contributor.author","Fries, L."],["dc.contributor.author","Goebbels, S."],["dc.contributor.author","Vreja, I. C."],["dc.contributor.author","Hagemeyer, N."],["dc.contributor.author","Dittrich, M."],["dc.contributor.author","Rossetti, M. F."],["dc.contributor.author","Kröhnert, K."],["dc.contributor.author","Hannke, K."],["dc.contributor.author","Boretius, S."],["dc.contributor.author","Zeug, A."],["dc.contributor.author","Höschen, C."],["dc.contributor.author","Dandekar, T."],["dc.contributor.author","Dere, E."],["dc.contributor.author","Neher, E."],["dc.contributor.author","Rizzoli, S. O."],["dc.contributor.author","Nave, K.-A."],["dc.contributor.author","Sirén, A.-L."],["dc.contributor.author","Ehrenreich, H."],["dc.date.accessioned","2017-09-07T11:53:29Z"],["dc.date.available","2017-09-07T11:53:29Z"],["dc.date.issued","2016"],["dc.description.abstract","Recombinant human erythropoietin (EPO) improves cognitive performance in neuropsychiatric diseases ranging from schizophrenia and multiple sclerosis to major depression and bipolar disease. This consistent EPO effect on cognition is independent of its role in hematopoiesis. The cellular mechanisms of action in brain, however, have remained unclear. Here we studied healthy young mice and observed that 3-week EPO administration was associated with an increased number of pyramidal neurons and oligodendrocytes in the hippocampus of ~20%. Under constant cognitive challenge, neuron numbers remained elevated until >6 months of age. Surprisingly, this increase occurred in absence of altered cell proliferation or apoptosis. After feeding a 15N-leucine diet, we used nanoscopic secondary ion mass spectrometry, and found that in EPO-treated mice, an equivalent number of neurons was defined by elevated 15N-leucine incorporation. In EPO-treated NG2-Cre-ERT2 mice, we confirmed enhanced differentiation of preexisting oligodendrocyte precursors in the absence of elevated DNA synthesis. A corresponding analysis of the neuronal lineage awaits the identification of suitable neuronal markers. In cultured neurospheres, EPO reduced Sox9 and stimulated miR124, associated with advanced neuronal differentiation. We are discussing a resulting working model in which EPO drives the differentiation of non-dividing precursors in both (NG2+) oligodendroglial and neuronal lineages. As endogenous EPO expression is induced by brain injury, such a mechanism of adult neurogenesis may be relevant for central nervous system regeneration."],["dc.identifier.doi","10.1038/mp.2015.212"],["dc.identifier.fs","620695"],["dc.identifier.gro","3145088"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14225"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2785"],["dc.language.iso","en"],["dc.notes.intern","Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","1359-4184"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Revisiting adult neurogenesis and the role of erythropoietin for neuronal and oligodendroglial differentiation in the hippocampus"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","eLife"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Patzig, Julia"],["dc.contributor.author","Erwig, Michelle S"],["dc.contributor.author","Tenzer, Stefan"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Schaeren-Wiemers, Nicole"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Werner, Hauke B"],["dc.date.accessioned","2021-06-01T10:48:59Z"],["dc.date.available","2021-06-01T10:48:59Z"],["dc.date.issued","2016"],["dc.description.abstract","Myelination of axons facilitates rapid impulse propagation in the nervous system. The axon/myelin-unit becomes impaired in myelin-related disorders and upon normal aging. However, the molecular cause of many pathological features, including the frequently observed myelin outfoldings, remained unknown. Using label-free quantitative proteomics, we find that the presence of myelin outfoldings correlates with a loss of cytoskeletal septins in myelin. Regulated by phosphatidylinositol-(4,5)-bisphosphate (PI(4,5)P2)-levels, myelin septins (SEPT2/SEPT4/SEPT7/SEPT8) and the PI(4,5)P2-adaptor anillin form previously unrecognized filaments that extend longitudinally along myelinated axons. By confocal microscopy and immunogold-electron microscopy, these filaments are localized to the non-compacted adaxonal myelin compartment. Genetic disruption of these filaments in Sept8-mutant mice causes myelin outfoldings as a very specific neuropathology. Septin filaments thus serve an important function in scaffolding the axon/myelin-unit, evidently a late stage of myelin maturation. We propose that pathological or aging-associated diminishment of the septin/anillin-scaffold causes myelin outfoldings that impair the normal nerve conduction velocity."],["dc.description.abstract","Normal communication within the brain or between the brain and other parts of the body requires information to flow quickly around the nervous system. This information travels along nerve cells in the form of electrical signals. To speed up the signals, a part of the nerve cell called the axon is frequently wrapped in an electrically insulating sheath made up of a membrane structure called myelin. The myelin sheath becomes impaired as a result of disease or ageing. In order to understand what might produce these changes, Patzig et al. have used biochemical and microscopy techniques to study mice that had similar defects in their myelin sheaths. The study reveals that forming a normal myelin sheath around an axon requires a newly identified ‘scaffold’ made of a group of proteins called the septins. Combining with another protein called anillin, septins assemble into filaments in the myelin sheath. These filaments then knit together into a scaffold that grows lengthways along the myelin-wrapped axon. Without this scaffold, the myelin sheath grew defects known as outfoldings. Axons transmitted electrical signals much more slowly than normal when the septin scaffold was missing from the myelin sheath. Future studies are needed to understand the factors that control how the septin scaffold forms. This could help to reveal ways of reversing the changes that alter the myelin sheath during ageing and disease."],["dc.identifier.doi","10.7554/eLife.17119"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13756"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86124"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2050-084X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Septin/anillin filaments scaffold central nervous system myelin to accelerate nerve conduction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2025"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","2040"],["dc.bibliographiccitation.volume","64"],["dc.contributor.author","Poggi, Giulia"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Moschny, Nicole"],["dc.contributor.author","Baudewig, Jürgen"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Hassouna, Imam"],["dc.contributor.author","Wieser, Georg L."],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:44:51Z"],["dc.date.available","2017-09-07T11:44:51Z"],["dc.date.issued","2016"],["dc.description.abstract","Subtle white matter abnormalities have emerged as a hallmark of brain alterations in magnetic resonance imaging or upon autopsy of mentally ill subjects. However, it is unknown whether such reduction of white matter and myelin contributes to any disease-relevant phenotype or simply constitutes an epiphenomenon, possibly even treatment-related. Here, we have re-analyzed Mbp heterozygous mice, the unaffected parental strain of shiverer, a classical neurological mutant. Between 2 and 20 months of age, Mbp+/- versus Mbp+/+ littermates were deeply phenotyped by combining extensive behavioral/cognitive testing with MRI, 1H-MR spectroscopy, electron microscopy, and molecular techniques. Surprisingly, Mbp-dependent myelination was significantly reduced in the prefrontal cortex. We also noticed a mild but progressive hypomyelination of the prefrontal corpus callosum and low-grade inflammation. While most behavioral functions were preserved, Mbp+/- mice exhibited defects of sensorimotor gating, as evidenced by reduced prepulse-inhibition, and a late-onset catatonia phenotype. Thus, subtle but primary abnormalities of CNS myelin can be the cause of a persistent cortical network dysfunction including catatonia, features typical of neuropsychiatric conditions."],["dc.identifier.doi","10.1002/glia.23039"],["dc.identifier.gro","3150347"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7101"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","0894-1491"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Cortical network dysfunction caused by a subtle defect of myelination"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e4286"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.contributor.author","Scheller, Anja"],["dc.contributor.author","Hirrlinger, Petra G."],["dc.contributor.author","Kellert, Beate"],["dc.contributor.author","Tang, Wannan"],["dc.contributor.author","Wehr, Michael C."],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Reichenbach, Andreas"],["dc.contributor.author","Sprengel, Rolf"],["dc.contributor.author","Rossner, Moritz J."],["dc.contributor.author","Kirchhoff, Frank"],["dc.date.accessioned","2019-07-09T11:53:56Z"],["dc.date.available","2019-07-09T11:53:56Z"],["dc.date.issued","2009-01-27"],["dc.description.abstract","Cre/LoxP recombination is the gold standard for conditional gene regulation in mice in vivo. However, promoters driving the expression of Cre recombinase are often active in a wide range of cell types and therefore unsuited to target more specific subsets of cells. To overcome this limitation, we designed inactive ‘‘split-Cre’’ fragments that regain Cre activity when overlapping co-expression is controlled by two different promoters. Using transgenic mice and virus-mediated expression of split-Cre, we show that efficient reporter gene activation is achieved in vivo. In the brain of transgenic mice, we genetically defined a subgroup of glial progenitor cells in which the Plp1- and the Gfap-promoter are simultaneously active, giving rise to both astrocytes and NG2-positive glia. Similarly, a subset of interneurons was labelled after viral transfection using Gad67- and Cck1 promoters to express split-Cre. Thus, split-Cre mediated genomic recombination constitutes a powerful spatial and temporal coincidence detector for in vivo targeting."],["dc.format.extent","10"],["dc.identifier.doi","10.1371/journal.pone.0004286"],["dc.identifier.pmid","19172189"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8268"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60531"],["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","Split-Cre Complementation Indicates Coincident Activity of Different Genes In Vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1001604"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLoS Biology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Fruehbeis, Carsten"],["dc.contributor.author","Froehlich, Dominik"],["dc.contributor.author","Kuo, Wen Ping"],["dc.contributor.author","Amphornrat, Jesa"],["dc.contributor.author","Thilemann, Sebastian"],["dc.contributor.author","Saab, Aiman S."],["dc.contributor.author","Kirchhoff, Frank"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Klugmann, Matthias"],["dc.contributor.author","Trotter, Jacqueline"],["dc.contributor.author","Kraemer-Albers, Eva-Maria"],["dc.date.accessioned","2018-11-07T09:22:56Z"],["dc.date.available","2018-11-07T09:22:56Z"],["dc.date.issued","2013"],["dc.description.abstract","Reciprocal interactions between neurons and oligodendrocytes are not only crucial for myelination, but also for long-term survival of axons. Degeneration of axons occurs in several human myelin diseases, however the molecular mechanisms of axon-glia communication maintaining axon integrity are poorly understood. Here, we describe the signal-mediated transfer of exosomes from oligodendrocytes to neurons. These endosome-derived vesicles are secreted by oligodendrocytes and carry specific protein and RNA cargo. We show that activity-dependent release of the neurotransmitter glutamate triggers oligodendroglial exosome secretion mediated by Ca2+ entry through oligodendroglial NMDA and AMPA receptors. In turn, neurons internalize the released exosomes by endocytosis. Injection of oligodendroglia-derived exosomes into the mouse brain results in functional retrieval of exosome cargo in neurons. Supply of cultured neurons with oligodendroglial exosomes improves neuronal viability under conditions of cell stress. These findings indicate that oligodendroglial exosomes participate in a novel mode of bidirectional neuron-glia communication contributing to neuronal integrity."],["dc.identifier.doi","10.1371/journal.pbio.1001604"],["dc.identifier.isi","000322592700008"],["dc.identifier.pmid","23874151"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9144"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29458"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1545-7885"],["dc.rights","CC BY-NC 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/3.0"],["dc.title","Neurotransmitter-Triggered Transfer of Exosomes Mediates Oligodendrocyte-Neuron Communication"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]