Aufgrund von Vorbereitungen auf eine neue Version von KOPS, können am Montag, 6.2. und Dienstag, 7.2. keine Publikationen eingereicht werden. (Due to preparations for a new version of KOPS, no publications can be submitted on Monday, Feb. 6 and Tuesday, Feb. 7.)
Type of Publication: | Journal article |
URI (citable link): | http://nbn-resolving.de/urn:nbn:de:bsz:352-opus-39018 |
Author: | Ankerhold, Richard; Stürmer, Claudia |
Year of publication: | 1999 |
Published in: | Journal of Neurobiology ; 41 (1999), 4. - pp. 572-584. - ISSN 0022-3034. - eISSN 1097-4695 |
DOI (citable link): | https://dx.doi.org/10.1002/(SICI)1097-4695(199912)41:4<572::AID-NEU12>3.0.CO;2-8 |
Summary: |
Retinal axons in goldfish regenerate after optic nerve lesion, restore synaptic connections, and become myelinated by oligodendrocytes. The fate of oligodendrocytes during these events is not known and may require generation of new oligodendrocytes or dedifferentiation and redifferentiation of the existing ones. To determine the reaction of oligodendrocytes to optic nerve lesion, we used the terminal transferase technique to detect apoptosis, bromodeoxyuridine incorporation to reveal mitosis, antibodies to identify myelin and oligodendrocytes, and Lucifer yellow injections to reveal cell morphology. Along with the reappearance of the myelin molecules 36K protein, galactocerebroside, and myelin basic protein, myelinating oligodendrocytes (identified by Lucifer yellow injections) reappear 21 days postlesion. Prior to this time, the dye-filled cells had few processes oriented along the regenerating axons. They resembled oligodendrocytes seen both in vitro and in vivo which express the L1-related E587 antigen and synthesize the 36K myelin protein in coculture with axons. No signs of oligodendrocyte apoptosis were detected after lesion and only few of the oligodendrocytes present had recently arisen. 36K/E587 double-labeled oligodendrocytes which were most likely dedifferentiating oligodendrocytes were identified in 8-day postlesion nerves among E587-positive elongate cells whose numbers increased until 14 days postlesion. These findings suggest that oligodendrocytes dedifferentiate like Schwann cells from cells which express myelin molecules to elongate cells which express the L1/E587 antigen. They redifferentiate to myelinate axons from roughly 3 weeks onward. These findings suggest an adaptive plasticity of goldfish oligodendrocytes beneficial to the repair of the visual pathway.
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Subject (DDC): | 570 Biosciences, Biology |
Keywords: | oligodendrocytes, adaptive plasticity, dedifferentiation, optic nerve lesion, axon regeneration, remyelination, adaptive plasticity, Schwann |
Link to License: | Attribution-NonCommercial-NoDerivs 2.0 Generic |
ANKERHOLD, Richard, Claudia STÜRMER, 1999. Fate of Oligodendrocytes during Retinal Axon Degeneration and Regeneration in the Goldfish Visual Pathway. In: Journal of Neurobiology. 41(4), pp. 572-584. ISSN 0022-3034. eISSN 1097-4695. Available under: doi: 10.1002/(SICI)1097-4695(199912)41:4<572::AID-NEU12>3.0.CO;2-8
@article{Ankerhold1999Oligo-6763, title={Fate of Oligodendrocytes during Retinal Axon Degeneration and Regeneration in the Goldfish Visual Pathway}, year={1999}, doi={10.1002/(SICI)1097-4695(199912)41:4<572::AID-NEU12>3.0.CO;2-8}, number={4}, volume={41}, issn={0022-3034}, journal={Journal of Neurobiology}, pages={572--584}, author={Ankerhold, Richard and Stürmer, Claudia} }
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Fate_of_oligodendrocytes.pdf | 577 |