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dc.contributor.advisor Keller, Bernhard Prof. Dr. de
dc.contributor.author Bergmann, Friederike de
dc.date.accessioned 2013-01-22T15:38:43Z de
dc.date.available 2013-01-30T23:50:58Z de
dc.date.issued 2004-03-03 de
dc.identifier.uri http://hdl.handle.net/11858/00-1735-0000-000D-F11F-0 de
dc.format.mimetype application/pdf de
dc.language.iso eng de
dc.rights.uri http://creativecommons.org/licenses/by-nc-nd/3.0/ de
dc.title Mitochondrial metabolism in hypoglossal motoneurons from mouse – implications for amyotrophic lateral sclerosis (ALS) de
dc.type doctoralThesis de
dc.title.translated Mitochondrialer Metabolismus in hypoglossalen Motoneuronen der Maus - Bedeutung für die Amyotrophe Lateral Sklerose (ALS) de
dc.contributor.referee Keller, Bernhard Prof. Dr. de
dc.date.examination 2004-02-12 de
dc.subject.gok MED 310 de
dc.description.abstracteng Motoneurons (MNs) are selectively damaged both in human amyotrophic lateral sclerosis (ALS) and corresponding mouse models of this neurodegenerative disease. A variety of studies indicate that mitochondrial dysfunction and disruption of the cellular Ca2+ homeostasis represent critical events during the disease process. Since little is known about the involvement of mitochondria in regulation of Ca2+ levels in MNs, the first aim of this work was to define the contribution of mitochondria to the clearance of physiological type Ca2+ loads. Second, the work aimed at characterizing the cellular consequences of mitochondrial dysfunction in MNs, with particular attention to changes in electrical properties and alterations in Ca2+ homeostasis, as this may give clues to the understanding of processes involved in MN degeneration and the selective vulnerability of MNs in ALS. The contribution of mitochondria to buffering of Ca2+ loads was investigated employing acute mouse brainstem slices containing the hypoglossal motor nucleus and CCD camera based imaging techniques. It was demonstrated that in hypoglossal MNs, mitochondria constitute the dominant Ca2+ clearance mechanism accounting for buffering of ~50 % of voltage activated Ca2+ loads with amplitudes below 0.4 de
dc.contributor.coReferee Paulus, Walter Prof. Dr. de
dc.contributor.thirdReferee Neher, Erwin Prof. Dr. de
dc.subject.topic Mathematics and Natural Science de
dc.subject.ger Motoneuron de
dc.subject.ger Mitochondrien de
dc.subject.ger Kalzium de
dc.subject.ger Neurodegeneration de
dc.subject.ger ALS de
dc.subject.ger Hypoxie de
dc.subject.ger Hypoglossus de
dc.subject.ger 570 Biowissenschaften de
dc.subject.ger Biologie de
dc.subject.eng motoneuron de
dc.subject.eng mitochondria de
dc.subject.eng calcium de
dc.subject.eng neurodegeneration de
dc.subject.eng ALS de
dc.subject.eng hypoxia de
dc.subject.eng hypoglossal de
dc.subject.bk 42.17 de
dc.subject.bk 42.15 de
dc.identifier.urn urn:nbn:de:gbv:7-webdoc-172-0 de
dc.identifier.purl webdoc-172 de
dc.identifier.ppn 502446064 de

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