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  Structural myelin defects are associated with low axonal ATP levels but rapid recovery from energy deprivation in a mouse model of spastic paraplegia

Trevisiol, A., Kusch, K., Steyer, A. M., Gregor, I., Nardis, C., Winkler, U., et al. (2020). Structural myelin defects are associated with low axonal ATP levels but rapid recovery from energy deprivation in a mouse model of spastic paraplegia. PLOS Biology, 18(11): e3000943. doi:10.1371/journal.pbio.3000943.

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Trevisiol, A.1, Author           
Kusch, K.1, Author           
Steyer, A. M.1, 2, Author           
Gregor, I., Author
Nardis, C.2, 3, Author           
Winkler, U., Author
Köhler, S., Author
Restrepo, A.1, Author           
Möbius, W.2, 3, Author           
Werner, H. B.1, Author           
Nave, K.-A.1, Author           
Hirrlinger, J.1, Author           
Monk, K. R., Editor
Affiliations:
1Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_2173664              
2Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_2173666              
3Electron microscopy, Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_2173666              

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 Abstract: In several neurodegenerative disorders, axonal pathology may originate from impaired oligodendrocyte-to-axon support of energy substrates. We previously established transgenic mice that allow measuring axonal ATP levels in electrically active optic nerves. Here, we utilize this technique to explore axonal ATP dynamics in the Plpnull/y mouse model of spastic paraplegia. Optic nerves from Plpnull/y mice exhibited lower and more variable basal axonal ATP levels and reduced compound action potential (CAP) amplitudes, providing a missing link between axonal pathology and a role of oligodendrocytes in brain energy metabolism. Surprisingly, when Plpnull/y optic nerves are challenged with transient glucose deprivation, both ATP levels and CAP decline slower, but recover faster upon reperfusion of glucose. Structurally, myelin sheaths display an increased frequency of cytosolic channels comprising glucose and monocarboxylate transporters, possibly facilitating accessibility of energy substrates to the axon. These data imply that complex metabolic alterations of the axon– myelin unit contribute to the phenotype of Plpnull/y mice.

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Language(s): eng - English
 Dates: 2020-11-16
 Publication Status: Published online
 Pages: 23
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 Rev. Type: -
 Identifiers: DOI: 10.1371/journal.pbio.3000943
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Title: PLOS Biology
Source Genre: Journal
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Pages: 23 Volume / Issue: 18 (11) Sequence Number: e3000943 Start / End Page: - Identifier: ISSN: 1545-7885