Suhr, Martin

[["dc.bibliographiccitation.artnumber","304"],["dc.bibliographiccitation.journal","Frontiers in Neuroscience"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Günther, R."],["dc.contributor.author","Saal, K.-A."],["dc.contributor.author","Suhr, M."],["dc.contributor.author","Scheer, D."],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Lingor, P."],["dc.contributor.author","Tönges, L."],["dc.date.accessioned","2017-09-07T11:45:27Z"],["dc.date.available","2017-09-07T11:45:27Z"],["dc.date.issued","2014"],["dc.description.abstract","Disease progression in amyotrophic lateral sclerosis (ALS) is characterized by degeneration of motoneurons and their axons which results in a progressive muscle weakness and ultimately death from respiratory failure. The only approved drug, riluzole, lacks clinical efficacy so that more potent treatment options are needed. We have identified rho kinase (ROCK) as a target, which can be manipulated to beneficially influence disease progression in models of ALS. Here, we examined the therapeutic potential of the ROCK inhibitor Y-27632 in both an in vitro and in an in vivo paradigm of motoneuron disease. Application of Y-27632 to primary motoneurons in vitro increased survival and promoted neunte outgrowth. In vivo, SOD1G93A mice were orally treated with 2 or 30 mg/kg body weight of Y-27632. The 2 mg/kg group did not benefit from Y-27632 treatment, whereas treatment with 30 mg/kg resulted in improved motor function in male mice. Female mice showed only limited improvement and overall survival was not modified in both 2 and 30 mg/kg Y-27632 groups. In conclusion, we provide evidence that inhibition of ROCK by Y-27632 is neuroprotective in vitro but has limited beneficial effects in vivo being restricted to male mice. Therefore, the evaluation of ROCK inhibitors in preclinical models of ALS should always take gender differences into account."],["dc.format.extent","9"],["dc.identifier.doi","10.3389/fnins.2014.00304"],["dc.identifier.gro","3142033"],["dc.identifier.isi","000346516800001"],["dc.identifier.pmid","25339858"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11029"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/3801"],["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","1662-453X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The rho kinase inhibitor Y-27632 improves motor performance in male SOD1(G93A) mice"],["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"]]

[["dc.bibliographiccitation.firstpage","425"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Molecular and Cellular Neuroscience"],["dc.bibliographiccitation.lastpage","431"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Hartelt, N."],["dc.contributor.author","Skorova, Ekaterina Y."],["dc.contributor.author","Manzke, Till"],["dc.contributor.author","Suhr, M."],["dc.contributor.author","Mironova, L."],["dc.contributor.author","Kuegler, Sebastian"],["dc.contributor.author","Mironov, Sergej L."],["dc.date.accessioned","2018-11-07T11:17:53Z"],["dc.date.available","2018-11-07T11:17:53Z"],["dc.date.issued","2008"],["dc.description.abstract","Topology of neuronal networks contributes to their functioning but the structure-function relationships are not yet understood. In order to reveal the spatial organisation of the respiratory network, we expressed enhanced green fluorescent proteins in neurons in brainstem slices containing the respiratory kernel (pre-Botzinger complex). The expression was neuron specific due to use of adeno-associated viral vector driving transgene expression from synapsin I promoter. Both neuronal cell bodies and their dendrites were labelled with high efficacy. This labelling allowed for enhanced spatial resolution as compared to conventional calcium-sensitive dyes. Neurons occupied about 10% of tissue volume and formed an interconnected network. Using custom-developed software, we quantified the network structure that had a modular structure consisting of clusters having transverse (dorsoventral) orientation. They contained in average seven neurons and connections between the cells in different clusters were less frequent. This novel in situ imaging technique is promising to gain new knowledge about the fine structure and function of neuronal networks in living slice preparations. (c) 2007 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.mcn.2007.10.011"],["dc.identifier.isi","000253928500001"],["dc.identifier.pmid","18203620"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54917"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","1044-7431"],["dc.title","Imaging of respiratory network topology in living brainstem slices"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e3936"],["dc.bibliographiccitation.issue","61"],["dc.bibliographiccitation.journal","Journal of Visualized Experiments"],["dc.contributor.author","Günther, R."],["dc.contributor.author","Suhr, M."],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Lingor, P."],["dc.contributor.author","Tönges, L."],["dc.date.accessioned","2017-09-07T11:48:58Z"],["dc.date.available","2017-09-07T11:48:58Z"],["dc.date.issued","2012"],["dc.description.abstract","Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder resulting in progressive degeneration of motoneurons. Peak of onset is around 60 years for the sporadic disease and around 50 years for the familial disease. Due to its progressive course, 50% of the patients die within 30 months of symptom onset. In order to evaluate novel treatment options for this disease, genetic mouse models of ALS have been generated based on human familial mutations in the SOD gene, such as the SOD1 (G93A) mutation. Most important aspects that have to be evaluated in the model are overall survival, clinical course and motor function. Here, we demonstrate the clinical evaluation, show the conduction of two behavioural motor tests and provide quantitative scoring systems for all parameters. Because an in depth analysis of the ALS mouse model usually requires an immunohistochemical examination of the spinal cord, we demonstrate its preparation in detail applying the dorsal laminectomy method. Exemplary histological findings are demonstrated. The comprehensive application of the depicted examination methods in studies on the mouse model of ALS will enable the researcher to reliably test future therapeutic options which can provide a basis for later human clinical trials."],["dc.identifier.doi","10.3791/3936"],["dc.identifier.gro","3142575"],["dc.identifier.isi","000209222800054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8941"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1940-087X"],["dc.title","Clinical Testing and Spinal Cord Removal in a Mouse Model for Amyotrophic Lateral Sclerosis (ALS)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","217"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","232"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Günther, R."],["dc.contributor.author","Suhr, M."],["dc.contributor.author","Jansen, J."],["dc.contributor.author","Balck, A."],["dc.contributor.author","Saal, K.-A."],["dc.contributor.author","Barski, E."],["dc.contributor.author","Nientied, T."],["dc.contributor.author","Götz, A. A."],["dc.contributor.author","Koch, J.-C."],["dc.contributor.author","Mueller, B. K."],["dc.contributor.author","Weishaupt, J. H."],["dc.contributor.author","Sereda, M. W."],["dc.contributor.author","Hanisch, U.-K."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Lingor, P."],["dc.date.accessioned","2017-09-07T11:46:53Z"],["dc.date.available","2017-09-07T11:46:53Z"],["dc.date.issued","2014"],["dc.description.abstract","Disease progression in amyotrophic lateral sclerosis (ALS) is characterized by degeneration of motoneurons (MN) and their axons, but is also influenced by neighboring cells such as astrocytes and microglial cells. The role of microglia in ALS is complex as it switches from an anti-inflammatory and neuroprotective phenotype in early disease to a proinflammatory and neurotoxic phenotype in later stages. Our previous studies in models of neurodegeneration identified rho kinase (ROCK) as a target, which can be manipulated to beneficially influence disease progression. Here, we examined the neuroprotective potential of the ROCK inhibitor Fasudil to target the central pathogenic features of ALS. Application of Fasudil to kainic acid-lesioned primary MN in vitro resulted in a strong prosurvival effect. In vivo, SOD1(G93A) mice benefited from oral treatment with Fasudil showing prolonged survival and improved motor function. These findings were correlated to an improved survival of motor neurons and a pronounced alteration of astroglial and microglial cell infiltration of the spinal cord under Fasudil treatment. Modeling a proinflammatory microglial phenotype by stimulation with LPS in vitro, Fasudil decreased the release of proinflammatory cytokines and chemokines TNF, Il6, CCL2, CCL3, and CCL5 while CXCL1 release was only transiently suppressed. In sciatic nerve motor axons, neuromuscular junction remodeling processes were increased. In conclusion, we provide preclinical and neurobiological evidence that inhibition of ROCK by the clinically approved small molecule inhibitor Fasudil may be a novel therapeutic approach in ALS combining both neuroprotection and immunomodulation for the cure of this devastating disease. GLIA 2014;62:217-232"],["dc.identifier.doi","10.1002/glia.22601"],["dc.identifier.gro","3142195"],["dc.identifier.isi","000328209300005"],["dc.identifier.pmid","24311453"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5588"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Rho Kinase Inhibition Modulates Microglia Activation and Improves Survival in a Model of Amyotrophic Lateral Sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Bioinformatics"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Suhr, M."],["dc.contributor.author","Lehmann, C."],["dc.contributor.author","Bauer, C. R."],["dc.contributor.author","Bender, T."],["dc.contributor.author","Knopp, C."],["dc.contributor.author","Freckmann, L."],["dc.contributor.author","Öst Hansen, B."],["dc.contributor.author","Henke, C."],["dc.contributor.author","Aschenbrandt, G."],["dc.contributor.author","Kühlborn, L. K."],["dc.contributor.author","Rheinländer, S."],["dc.contributor.author","Weber, L."],["dc.contributor.author","Marzec, B."],["dc.contributor.author","Hellkamp, M."],["dc.contributor.author","Wieder, P."],["dc.contributor.author","Sax, U."],["dc.contributor.author","Kusch, H."],["dc.contributor.author","Nussbeck, S. Y."],["dc.date.accessioned","2021-04-14T08:32:27Z"],["dc.date.available","2021-04-14T08:32:27Z"],["dc.date.issued","2020"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.1186/s12859-020-03928-1"],["dc.identifier.pmid","33334310"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17711"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83924"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/374"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/132"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | INF: Unterstützung der SFB 1002 Forschungsdatenintegration, -visualisierung und -nachnutzung"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | Z03: Synthetische genetische Analyse, automatisierte Mikroskopie und Bildanalyse"],["dc.relation.eissn","1471-2105"],["dc.relation.orgunit","Gesellschaft für wissenschaftliche Datenverarbeitung"],["dc.relation.workinggroup","RG Nußbeck"],["dc.relation.workinggroup","RG Schwappach (Membrane Protein Biogenesis)"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Menoci: lightweight extensible web portal enhancing data management for biomedical research projects"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]