Modulation der Hypoxie-Empfindlichkeit medullärer Netzwerke in einem Maus-Modell des Rett-Syndroms

Zimmermann, Jasper Lukas

dc.contributor.advisor	Müller, Michael Prof. Dr.	de
dc.contributor.author	Zimmermann, Jasper Lukas	de
dc.date.accessioned	2013-01-14T15:31:09Z	de
dc.date.available	2013-01-30T23:50:53Z	de
dc.date.issued	2012-09-14	de
dc.identifier.uri	http://hdl.handle.net/11858/00-1735-0000-000D-F009-8	de
dc.identifier.uri	http://dx.doi.org/10.53846/goediss-1610
dc.format.mimetype	application/pdf	de
dc.language.iso	ger	de
dc.rights.uri	http://creativecommons.org/licenses/by-nc-nd/3.0/	de
dc.title	Modulation der Hypoxie-Empfindlichkeit medullärer Netzwerke in einem Maus-Modell des Rett-Syndroms	de
dc.type	doctoralThesis	de
dc.title.translated	Modulation of hypoxia-susceptibility of medullary networks in a mouse-modell of Rett-syndrome	de
dc.contributor.referee	Müller, Michael Prof. Dr.	de
dc.date.examination	2012-02-14	de
dc.subject.dnb	610 Medizin, Gesundheit	de
dc.subject.gok	MED 311	de
dc.description.abstracteng	For this thesis I investigated if elicitation of hypoxia-induced spreading depression-like depolarizations (HSDs) in the brain stem of mice is possible. Furthermore I screened for differences in hypoxia susceptibility between Mecp2-/y- and wildtype-mice and whether hypoxia susceptibility could be influenced by 5-HT1A-receptor agonist 8-OH-DPAT. In addition I investigated the direct influence of HSDs on breathing-associated medullary rhythmic activity. Results show that HSDs can consistently be elicitated in brain stem of juvenile (p10-15) mice. Furthermore I detected an enhanced hypoxia susceptibility in Mecp2-/y-mice a mouse model for Rett syndrome. To investigate the influence of HSDs on medullary respiratory rhythm genesis I adapted the preparation of rhythmically active brain stem slices to interface chamber conditions. This allowed analysis of rhythmic brain stem activity at almost physiological conditions. Analysis of rhythmically active slices showed a complete reversible blockage of rhythmic activity upon occurrence of a HSDs. Combined with the results regarding an enhanced hypoxia susceptibility of these brainstem areas in Mecp2-/y-mice this might be a possible account for the often letal apneas in Mecp2-/y-mice as well as human Rett patients. Furthermore my results support the thesis that HSDs in brainstem might be a possible explanation for sudden infant death syndrome. By adding 50	de
dc.contributor.coReferee	Huppke, Peter Prof. Dr.	de
dc.subject.topic	Medicine	de
dc.subject.ger	Hirnstamm	de
dc.subject.ger	Rett-Syndrom	de
dc.subject.ger	Mecp2	de
dc.subject.ger	Hypoxie	de
dc.subject.ger	SIDS	de
dc.subject.ger	plötzlicher Kindstod	de
dc.subject.ger	Serotonin	de
dc.subject.eng	brain stem	de
dc.subject.eng	Rett syndrome	de
dc.subject.eng	Mecp2	de
dc.subject.eng	hypoxia	de
dc.subject.eng	sudden infant death syndrome	de
dc.subject.eng	serotonine	de
dc.subject.bk	44.37	de
dc.identifier.urn	urn:nbn:de:gbv:7-webdoc-3691-1	de
dc.identifier.purl	webdoc-3691	de
dc.affiliation.institute	Medizinische Fakultät	de
dc.identifier.ppn	732056721	de

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Human- und Zahnmedizin [2872]

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