Molecular mechanisms of acute axonal degeneration in the rat optic nerve

Zhang, Jiannan

dc.contributor.advisor	Heinrich, Ralf Prof. Dr.
dc.contributor.author	Zhang, Jiannan
dc.date.accessioned	2015-12-03T09:06:57Z
dc.date.available	2016-11-10T23:50:05Z
dc.date.issued	2015-12-03
dc.identifier.uri	http://hdl.handle.net/11858/00-1735-0000-0028-8657-9
dc.identifier.uri	http://dx.doi.org/10.53846/goediss-5410
dc.language.iso	eng	de
dc.rights.uri	http://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.ddc	570	de
dc.title	Molecular mechanisms of acute axonal degeneration in the rat optic nerve	de
dc.type	doctoralThesis	de
dc.contributor.referee	Heinrich, Ralf Prof. Dr.
dc.date.examination	2015-11-11
dc.description.abstracteng	The development of neuroprotective treatments is urgently needed for neurodegenerative and neurotraumatic diseases. As axonal degeneration is a key initiating event in these diseases, it is pivotal to better understand and counteract axonal degeneration. A traumatic lesion of axons in the central nervous system is followed by acute axonal degeneration (AAD) within several hours. However, the underlying molecular mechanisms of AAD are still incompletely understood. The aim of this study was to investigate the mechanisms of AAD following calcium influx after optic nerve crush in vivo and after axotomy of cortical neurons in the microfluidic chamber system in vitro. A continuous increase in calpain activity was demonstrated following calcium influx. Calpain then cleaved collapsin response mediator protein (CRMP2), which impaired mitochondrial transport. Both calpain inhibition and CRMP2 overexpression almost completely inhibited axonal fragmentation proximal to the lesion site during AAD. Finally, several CRMP2-interacting partners were regulated during AAD and might contribute to AAD.	de
dc.contributor.coReferee	Hörner, Michael Prof. Dr.
dc.subject.eng	axonal degeneration	de
dc.subject.eng	calpain	de
dc.subject.eng	cortical neuron	de
dc.subject.eng	CRMP2	de
dc.subject.eng	microfluidic chamber	de
dc.subject.eng	mitochondrial transport	de
dc.subject.eng	optic nerve	de
dc.identifier.urn	urn:nbn:de:gbv:7-11858/00-1735-0000-0028-8657-9-5
dc.affiliation.institute	Biologische Fakultät für Biologie und Psychologie	de
dc.subject.gokfull	Biologie (PPN619462639)	de
dc.description.embargoed	2016-11-10
dc.identifier.ppn	842118489

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