Müller, Michael

[["dc.bibliographiccitation.artnumber","479"],["dc.bibliographiccitation.journal","Frontiers in Physiology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Can, Karolina"],["dc.contributor.author","Menzfeld, Christiane"],["dc.contributor.author","Rinne, Lena"],["dc.contributor.author","Rehling, Peter"],["dc.contributor.author","Kügler, Sebastian"],["dc.contributor.author","Golubiani, Gocha"],["dc.contributor.author","Dudek, Jan"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2019-07-09T11:51:15Z"],["dc.date.available","2019-07-09T11:51:15Z"],["dc.date.issued","2019"],["dc.description.abstract","Rett syndrome (RTT), an X chromosome-linked neurodevelopmental disorder affecting almost exclusively females, is associated with various mitochondrial alterations. Mitochondria are swollen, show altered respiratory rates, and their inner membrane is leaking protons. To advance the understanding of these disturbances and clarify their link to redox impairment and oxidative stress, we assessed mitochondrial respiration in defined brain regions and cardiac tissue of male wildtype (WT) and MeCP2-deficient (Mecp2-/y) mice. Also, we quantified for the first time neuronal redox-balance with subcellular resolution in cytosol and mitochondrial matrix. Quantitative roGFP1 redox imaging revealed more oxidized conditions in the cytosol of Mecp2-/y hippocampal neurons than in WT neurons. Furthermore, cytosol and mitochondria of Mecp2-/y neurons showed exaggerated redox-responses to hypoxia and cell-endogenous reactive oxygen species (ROS) formation. Biochemical analyzes exclude disease-related increases in mitochondrial mass in Mecp2-/y hippocampus and cortex. Protein levels of complex I core constituents were slightly lower in Mecp2-/y hippocampus and cortex than in WT; those of complex V were lower in Mecp2-/y cortex. Respiratory supercomplex-formation did not differ among genotypes. Yet, supplied with the complex II substrate succinate, mitochondria of Mecp2-/y cortex and hippocampus consumed more O2 than WT. Furthermore, mitochondria from Mecp2-/y hippocampus and cortex mediated an enhanced oxidative burden. In conclusion, we further advanced the molecular understanding of mitochondrial dysfunction in RTT. Intensified mitochondrial O2 consumption, increased mitochondrial ROS generation and disturbed redox balance in mitochondria and cytosol may represent a causal chain, which provokes dysregulated proteins, oxidative tissue damage, and contributes to neuronal network dysfunction in RTT."],["dc.identifier.doi","10.3389/fphys.2019.00479"],["dc.identifier.pmid","31114506"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16085"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59907"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/12"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | A06: Mitochondrienfunktion und -umsatz in Synapsen"],["dc.relation.workinggroup","RG Rehling (Mitochondrial Protein Biogenesis)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","573"],["dc.subject.ddc","612"],["dc.title","Neuronal Redox-Imbalance in Rett Syndrome Affects Mitochondria as Well as Cytosol, and Is Accompanied by Intensified Mitochondrial O2 Consumption and ROS Release"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","56"],["dc.bibliographiccitation.journal","Frontiers in Cellular Neuroscience"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Janc, Oliwia A."],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2018-09-28T10:14:12Z"],["dc.date.available","2018-09-28T10:14:12Z"],["dc.date.issued","2014"],["dc.description.abstract","Rett syndrome (RS) causes severe cognitive impairment, loss of speech, epilepsy, and breathing disturbances with intermittent hypoxia. Also mitochondria are affected; a subunit of respiratory complex III is dysregulated, the inner mitochondrial membrane is leaking protons, and brain ATP levels seem reduced. Our recent assessment of mitochondrial function in MeCP2 (methyl-CpG-binding protein 2)-deficient mouse (Mecp2 (-) (/y)) hippocampus confirmed early metabolic alterations, an increased oxidative burden, and a more vulnerable cellular redox balance. As these changes may contribute to the manifestation of symptoms and disease progression, we now evaluated whether free radical scavengers are capable of improving neuronal and mitochondrial function in RS. Acute hippocampal slices of adult mice were incubated with the vitamin E derivative Trolox for 3-5 h. In Mecp2 (-) (/y) slices this treatment dampened neuronal hyperexcitability, improved synaptic short-term plasticity, and fully restored synaptic long-term potentiation (LTP). Furthermore, Trolox specifically attenuated the increased hypoxia susceptibility of Mecp2 (-) (/y) slices. Also, the anticonvulsive effects of Trolox were assessed, but the severity of 4-aminopyridine provoked seizure-like discharges was not significantly affected. Adverse side effects of Trolox on mitochondria can be excluded, but clear indications for an improvement of mitochondrial function were not found. Since several ion-channels and neurotransmitter receptors are redox modulated, the mitochondrial alterations and the associated oxidative burden may contribute to the neuronal dysfunction in RS. We confirmed in Mecp2 (-) (/y) hippocampus that Trolox dampens neuronal hyperexcitability, reinstates synaptic plasticity, and improves the hypoxia tolerance. Therefore, radical scavengers are promising compounds for the treatment of neuronal dysfunction in RS and deserve further detailed evaluation."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2014"],["dc.identifier.doi","10.3389/fncel.2014.00056"],["dc.identifier.pmid","24605086"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9944"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15854"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","The free radical scavenger Trolox dampens neuronal hyperexcitability, reinstates synaptic plasticity, and improves hypoxia tolerance in a mouse model of Rett syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2915"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","2930"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Kobe, Fritz"],["dc.contributor.author","Guseva, Daria"],["dc.contributor.author","Jensen, Thomas P."],["dc.contributor.author","Wirth, Alexander"],["dc.contributor.author","Renner, Ute"],["dc.contributor.author","Hess, Dietmar"],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Medrihan, Lucian"],["dc.contributor.author","Zhang, Weiqi"],["dc.contributor.author","Zhang, Mingyue"],["dc.contributor.author","Braun, Katharina"],["dc.contributor.author","Westerholz, Sören"],["dc.contributor.author","Herzog, Andreas"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Richter, Diethelm W."],["dc.contributor.author","Rusakov, Dmitri A."],["dc.contributor.author","Ponimaskin, Evgeni"],["dc.date.accessioned","2017-09-07T11:46:22Z"],["dc.date.available","2017-09-07T11:46:22Z"],["dc.date.issued","2012"],["dc.description.abstract","The common neurotransmitter serotonin controls different aspects of early neuronal differentiation, although the underlying mechanisms are poorly understood. Here we report that activation of the serotonin 5-HT7 receptor promotes synaptogenesis and enhances synaptic activity in hippocampal neurons at early postnatal stages. An analysis of Gα12-deficient mice reveals a critical role of G12-protein for 5-HT7 receptor-mediated effects in neurons. In organotypic preparations from the hippocampus of juvenile mice, stimulation of 5-HT7R/G12 signaling potentiates formation of dendritic spines, increases neuronal excitability, and modulates synaptic plasticity. In contrast, in older neuronal preparations, morphogenetic and synaptogenic effects of 5-HT7/G12 signaling are abolished. Moreover, inhibition of 5-HT7 receptor had no effect on synaptic plasticity in hippocampus of adult animals. Expression analysis reveals that the production of 5-HT7 and Gα12-proteins in the hippocampus undergoes strong regulation with a pronounced transient increase during early postnatal stages. Thus, regulated expression of 5-HT7 receptor and Gα12-protein may represent a molecular mechanism by which serotonin specifically modulates formation of initial neuronal networks during early postnatal development."],["dc.identifier.doi","10.1523/JNEUROSCI.2765-11.2012"],["dc.identifier.gro","3150488"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7258"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.title","5-HT₇R/G₁₂ signaling regulates neuronal morphology and function in an age-dependent manner"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","53"],["dc.bibliographiccitation.journal","Frontiers in Pharmacology"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Schnell, Christian"],["dc.contributor.author","Janc, Oliwia A."],["dc.contributor.author","Kempkes, Belinda"],["dc.contributor.author","Araya Callis, Carolina"],["dc.contributor.author","Flügge, Gabriele"],["dc.contributor.author","Hülsmann, Swen"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2018-09-28T10:22:20Z"],["dc.date.available","2018-09-28T10:22:20Z"],["dc.date.issued","2012"],["dc.description.abstract","Chronic stress affects neuronal networks by inducing dendritic retraction, modifying neuronal excitability and plasticity, and modulating glial cells. To elucidate the functional consequences of chronic stress for the hippocampal network, we submitted adult rats to daily restraint stress for 3 weeks (6 h/day). In acute hippocampal tissue slices of stressed rats, basal synaptic function and short-term plasticity at Schaffer collateral/CA1 neuron synapses were unchanged while long-term potentiation was markedly impaired. The spatiotemporal propagation pattern of hypoxia-induced spreading depression episodes was indistinguishable among control and stress slices. However, the duration of the extracellular direct current potential shift was shortened after stress. Moreover, K(+) fluxes early during hypoxia were more intense, and the postsynaptic recoveries of interstitial K(+) levels and synaptic function were slower. Morphometric analysis of immunohistochemically stained sections suggested hippocampal shrinkage in stressed rats, and the number of cells that are immunoreactive for glial fibrillary acidic protein was increased in the CA1 subfield indicating activation of astrocytes. Western blots showed a marked downregulation of the inwardly rectifying K(+) channel Kir4.1 in stressed rats. Yet, resting membrane potentials, input resistance, and K(+)-induced inward currents in CA1 astrocytes were indistinguishable from controls. These data indicate an intensified interstitial K(+) accumulation during hypoxia in the hippocampus of chronically stressed rats which seems to arise from a reduced interstitial volume fraction rather than impaired glial K(+) buffering. One may speculate that chronic stress aggravates hypoxia-induced pathophysiological processes in the hippocampal network and that this has implications for the ischemic brain."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2012"],["dc.identifier.doi","10.3389/fphar.2012.00053"],["dc.identifier.pmid","22470344"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7501"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15856"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1663-9812"],["dc.rights","CC BY-NC 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/3.0"],["dc.title","Restraint Stress Intensifies Interstitial K(+) Accumulation during Severe Hypoxia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","27"],["dc.bibliographiccitation.journal","BMC Biology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Sargin, Derya"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Agarwal, Amit"],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Wojcik, Sonja M."],["dc.contributor.author","Hassouna, Imam"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:35Z"],["dc.date.available","2017-09-07T11:46:35Z"],["dc.date.issued","2011"],["dc.description.abstract","BACKGROUND: Erythropoietin (EPO) and its receptor (EPOR) are expressed in the developing brain and their transcription is upregulated in adult neurons and glia upon injury or neurodegeneration. We have shown neuroprotective effects and improved cognition in patients with neuropsychiatric diseases treated with EPO. However, the critical EPO targets in brain are unknown, and separation of direct and indirect effects has remained difficult, given the role of EPO in hematopoiesis and brain oxygen supply. RESULTS: Here we demonstrate that mice with transgenic expression of a constitutively active EPOR isoform (cEPOR) in pyramidal neurons of cortex and hippocampus exhibit enhancement of spatial learning, cognitive flexibility, social memory, and attentional capacities, accompanied by increased impulsivity. Superior cognitive performance is associated with augmented long-term potentiation of cEPOR expressing neurons in hippocampal slices. CONCLUSIONS: Active EPOR stimulates neuronal plasticity independent of any hematopoietic effects and in addition to its neuroprotective actions. This property of EPOR signaling should be exploited for defining novel strategies to therapeutically enhance cognitive performance in disease conditions."],["dc.format.extent","16"],["dc.identifier.doi","10.1186/1741-7007-9-27"],["dc.identifier.gro","3150548"],["dc.identifier.pmid","21527022"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6376"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7322"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Expression of constitutively active erythropoietin receptor in pyramidal neurons of cortex and hippocampus boosts higher cognitive functions in 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","2539"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Festerling, Karina"],["dc.contributor.author","Can, Karolina"],["dc.contributor.author","Kügler, Sebastian"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2021-04-14T08:26:49Z"],["dc.date.available","2021-04-14T08:26:49Z"],["dc.date.issued","2020"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.identifier.doi","10.3390/cells9122539"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17668"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82087"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","MDPI"],["dc.relation.eissn","2073-4409"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Overshooting Subcellular Redox-Responses in Rett-Mouse Hippocampus during Neurotransmitter Stimulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Antioxidants"],["dc.bibliographiccitation.volume","11"],["dc.contributor.affiliation","Baroncelli, Laura; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.affiliation","Auel, Stefanie; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.affiliation","Rinne, Lena; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.affiliation","Schuster, Ann-Kathrin; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.affiliation","Brand, Victoria; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.affiliation","Kempkes, Belinda; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.affiliation","Dietrich, Katharina; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.affiliation","Müller, Michael; 1Institut für Neuro- und Sinnesphysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany; laura.baroncelli@in.cnr.it (L.B.); stefanieauel@yahoo.de (S.A.); lena.rinne@gmx.net (L.R.); ak_schuster@web.de (A.-K.S.); victoriabrand@gmx.de (V.B.); bhildeb2@gwdg.de (B.K.); dietrich.katharina85@gmail.com (K.D.)"],["dc.contributor.author","Baroncelli, Laura"],["dc.contributor.author","Auel, Stefanie"],["dc.contributor.author","Rinne, Lena"],["dc.contributor.author","Schuster, Ann-Kathrin"],["dc.contributor.author","Brand, Victoria"],["dc.contributor.author","Kempkes, Belinda"],["dc.contributor.author","Dietrich, Katharina"],["dc.contributor.author","Müller, Michael"],["dc.date.accessioned","2022-08-04T08:23:31Z"],["dc.date.available","2022-08-04T08:23:31Z"],["dc.date.issued","2022-07-20"],["dc.date.updated","2022-08-03T09:14:27Z"],["dc.description.abstract","Rett syndrome (RTT) is a severe neurodevelopmental disorder that typically arises from spontaneous germline mutations in the X-chromosomal methyl-CpG binding protein 2 (MECP2) gene. For the first 6–18 months of life, the development of the mostly female patients appears normal. Subsequently, cognitive impairment, motor disturbances, hand stereotypies, epilepsy, and irregular breathing manifest, with previously learned skills being lost. Early mitochondrial impairment and a systemic oxidative burden are part of the complex pathogenesis, and contribute to disease progression. Accordingly, partial therapeutic merits of redox-stabilizing and antioxidant (AO) treatments were reported in RTT patients and Mecp2-mutant mice. Pursuing these findings, we conducted a full preclinical trial on male and female mice to define the therapeutic value of an orally administered AO cocktail composed of vitamin E, N-acetylcysteine, and α-lipoic acid. AO treatment ameliorated some of the microcephaly-related aspects. Moreover, the reduced growth, lowered blood glucose levels, and the hippocampal synaptic plasticity of Mecp2−/y mice improved. However, the first-time detected intensified oxidative DNA damage in Mecp2-mutant cortex persisted. The behavioral performance, breathing regularity, and life expectancy of Mecp2-mutant mice did not improve upon AO treatment. Long-term-treated Mecp2+/− mice eventually became obese. In conclusion, the AO cocktail ameliorated a subset of symptoms of the complex RTT-related phenotype, thereby further confirming the potential merits of AO-based pharmacotherapies. Yet, it also became evident that long-term AO treatment may lose efficacy and even aggravate the metabolic disturbances in RTT. This emphasizes the importance of a constantly well-balanced redox balance for systemic well-being."],["dc.description.sponsorship","Cluster of Excellence and Deutsche Forschungsgemeinschaft Research Center Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB)"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG, German Research Foundation)"],["dc.description.sponsorship","Umberto Veronesi Foundation"],["dc.description.sponsorship","Georg-August-Universität Göttingen"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3390/antiox11071406"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112622"],["dc.language.iso","en"],["dc.relation.eissn","2076-3921"],["dc.rights","CC BY 4.0"],["dc.title","Oral Feeding of an Antioxidant Cocktail as a Therapeutic Strategy in a Mouse Model of Rett Syndrome: Merits and Limitations of Long-Term Treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1089"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Geburtshilfe und Frauenheilkunde"],["dc.bibliographiccitation.lastpage","1109"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Emons, Günter"],["dc.contributor.author","Steiner, Eric"],["dc.contributor.author","Vordermark, Dirk"],["dc.contributor.author","Uleer, Christoph"],["dc.contributor.author","Bock, Nina"],["dc.contributor.author","Paradies, Kerstin"],["dc.contributor.author","Ortmann, Olaf"],["dc.contributor.author","Aretz, Stefan"],["dc.contributor.author","Mallmann, Peter"],["dc.contributor.author","Kurzeder, Christian"],["dc.contributor.author","Hagen, Volker"],["dc.contributor.author","van Oorschot, Birgitt"],["dc.contributor.author","Höcht, Stefan"],["dc.contributor.author","Feyer, Petra"],["dc.contributor.author","Egerer, Gerlinde"],["dc.contributor.author","Friedrich, Michael"],["dc.contributor.author","Cremer, Wolfgang"],["dc.contributor.author","Prott, Franz-Josef"],["dc.contributor.author","Horn, Lars-Christian"],["dc.contributor.author","Prömpeler, Heinrich"],["dc.contributor.author","Langrehr, Jan"],["dc.contributor.author","Leinung, Steffen"],["dc.contributor.author","Beckmann, Matthias"],["dc.contributor.author","Kimmig, Rainer"],["dc.contributor.author","Letsch, Anne"],["dc.contributor.author","Reinhardt, Michael"],["dc.contributor.author","Alt-Epping, Bernd"],["dc.contributor.author","Kiesel, Ludwig"],["dc.contributor.author","Menke, Jan"],["dc.contributor.author","Gebhardt, Marion"],["dc.contributor.author","Steinke-Lange, Verena"],["dc.contributor.author","Rahner, Nils"],["dc.contributor.author","Lichtenegger, Werner"],["dc.contributor.author","Zeimet, Alain"],["dc.contributor.author","Hanf, Volker"],["dc.contributor.author","Weis, Joachim"],["dc.contributor.author","Mueller, Michael"],["dc.contributor.author","Henscher, Ulla"],["dc.contributor.author","Schmutzler, Rita"],["dc.contributor.author","Meindl, Alfons"],["dc.contributor.author","Hilpert, Felix"],["dc.contributor.author","Panke, Joan"],["dc.contributor.author","Strnad, Vratislav"],["dc.contributor.author","Niehues, Christiane"],["dc.contributor.author","Dauelsberg, Timm"],["dc.contributor.author","Niehoff, Peter"],["dc.contributor.author","Mayr, Doris"],["dc.contributor.author","Grab, Dieter"],["dc.contributor.author","Kreißl, Michael"],["dc.contributor.author","Witteler, Ralf"],["dc.contributor.author","Schorsch, Annemarie"],["dc.contributor.author","Mustea, Alexander"],["dc.contributor.author","Petru, Edgar"],["dc.contributor.author","Hübner, Jutta"],["dc.contributor.author","Rose, Anne"],["dc.contributor.author","Wight, Edward"],["dc.contributor.author","Tholen, Reina"],["dc.contributor.author","Bauerschmitz, Gerd"],["dc.contributor.author","Fleisch, Markus"],["dc.contributor.author","Juhasz-Boess, Ingolf"],["dc.contributor.author","Lax, Sigurd"],["dc.contributor.author","Runnebaum, Ingo"],["dc.contributor.author","Tempfer, Clemens"],["dc.contributor.author","Nothacker, Monika"],["dc.contributor.author","Blödt, Susanne"],["dc.contributor.author","Follmann, Markus"],["dc.contributor.author","Langer, Thomas"],["dc.contributor.author","Raatz, Heike"],["dc.contributor.author","Wesselmann, Simone"],["dc.contributor.author","Erdogan, Saskia"],["dc.date.accessioned","2020-12-10T18:12:05Z"],["dc.date.available","2020-12-10T18:12:05Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1055/a-0715-2964"],["dc.identifier.eissn","1438-8804"],["dc.identifier.issn","0016-5751"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/74238"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Interdisciplinary Diagnosis, Therapy and Follow-up of Patients with Endometrial Cancer. Guideline (S3-Level, AWMF Registry Number 032/034-OL, April 2018) – Part 2 with Recommendations on the Therapy and Follow-up of Endometrial Cancer, Palliative Care, Psycho-oncological/Psychosocial Care/Rehabilitation/Patient Information and Healthcare Facilities"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","959"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Biochemical Society Transactions"],["dc.bibliographiccitation.lastpage","964"],["dc.bibliographiccitation.volume","42"],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Can, Karolina"],["dc.date.accessioned","2018-09-28T10:11:26Z"],["dc.date.available","2018-09-28T10:11:26Z"],["dc.date.issued","2014"],["dc.description.abstract","RTT (Rett syndrome) is a severe progressive neurodevelopmental disorder with a monogenetic cause, but complex and multifaceted clinical appearance. Compelling evidence suggests that mitochondrial alterations and aberrant redox homoeostasis result in oxidative challenge. Yet, compared with other severe neuropathologies, RTT is not associated with marked neurodegeneration, but rather a chemical imbalance and miscommunication of neuronal elements. Different pharmacotherapies mediate partial improvement of conditions in RTT, and also antioxidants or compounds improving mitochondrial function may be of potential merit. In the present paper, we summarize findings from patients and transgenic mice that point towards the nature of RTT as a mitochondrial disease. Also, open questions are addressed that require clarification to fully understand and successfully target the associated cellular redox imbalance."],["dc.identifier.doi","10.1042/BST20140071"],["dc.identifier.pmid","25109986"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15853"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1470-8752"],["dc.title","Aberrant redox homoeostasis and mitochondrial dysfunction in Rett syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","309"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","319"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","Gerchen, Martin F."],["dc.contributor.author","Adamcio, Bartosz"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Martin, Sabine"],["dc.contributor.author","Malzahn, Dörthe"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Radyushkin, Konstantin A."],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Benseler, Fritz"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:44:13Z"],["dc.date.available","2017-09-07T11:44:13Z"],["dc.date.issued","2011"],["dc.description.abstract","KCNN3, encoding the small conductance calcium-activated potassium channel SK3, harbours a polymorphic CAG repeat in the amino-terminal coding region with yet unproven function. Hypothesizing that KCNN3 genotypes do not influence susceptibility to schizophrenia but modify its phenotype, we explored their contribution to specific schizophrenic symptoms. Using the Gottingen Research Association for Schizophrenia (GRAS) data collection of schizophrenic patients (n=1074), we performed a phenotype-based genetic association study (PGAS) of KCNN3. We show that long CAG repeats in the schizophrenic sample are specifically associated with better performance in higher cognitive tasks, comprising the capacity to discriminate, select and execute (p<0.0001). Long repeats reduce SK3 channel function, as we demonstrate by patch-clamping of transfected HEK293 cells. In contrast, modelling the opposite in mice, i.e. KCNN3 overexpression/channel hyperfunction, leads to selective deficits in higher brain functions comparable to those influenced by SK3 conductance in humans. To conclude, KCNN3 genotypes modify cognitive performance, shown here in a large sample of schizophrenic patients. Reduction of SK3 function may constitute a pharmacological target to improve cognition in schizophrenia and other conditions with cognitive impairment."],["dc.identifier.doi","10.1002/emmm.201100135"],["dc.identifier.gro","3142723"],["dc.identifier.isi","000292277600003"],["dc.identifier.pmid","21433290"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8179"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/159"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1757-4676"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A CAG repeat polymorphism of KCNN3 predicts SK3 channel function and cognitive performance in schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]