Early onset of degenerative changes at nodes of Ranvier in alpha-motor axons of Cntf null (−/−) mutant mice

The nodes of Ranvier are sites of specific interaction between Schwann cells and axons. Besides their crucial role in transmission of action potentials, the nodes of Ranvier and in particular the paranodal axon‐Schwann cell networks (ASNs) are thought to function as local centers in large motor axon...

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Published in:	Glia Vol. 42; no. 4; pp. 340 - 349
Main Authors:	Gatzinsky, Kliment P., Holtmann, Bettina, Daraie, Babak, Berthold, Claes-Henric, Sendtner, Michael
Format:	Journal Article
Language:	English
Published:	New York Wiley Subscription Services, Inc., A Wiley Company 01-06-2003 Wiley-Liss
Subjects:	Animals axon-Schwann cell network Axons - pathology Axons - ultrastructure Biological and medical sciences Ciliary Neurotrophic Factor - deficiency Ciliary Neurotrophic Factor - genetics Fundamental and applied biological sciences. Psychology Isolated neuron and nerve. Neuroglia Male Mice Mice, Knockout Microscopy, Electron motor neuron Motor Neurons - pathology Motor Neurons - ultrastructure Nerve Degeneration - pathology nerve fiber paranode Ranvier's Nodes - pathology Ranvier's Nodes - ultrastructure Schwann Cells - pathology Schwann Cells - ultrastructure Spinal Nerve Roots - pathology ventral root Vertebrates: nervous system and sense organs Neuroglia Rodentia axon-Schwann cell network Axon ventral root Motor neuron Ciliary neurotrophic factor paranode Vertebrata Mammalia Mouse Schwann cell nerve fiber Node of Ranvier Degeneration Mutation
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Summary:	The nodes of Ranvier are sites of specific interaction between Schwann cells and axons. Besides their crucial role in transmission of action potentials, the nodes of Ranvier and in particular the paranodal axon‐Schwann cell networks (ASNs) are thought to function as local centers in large motor axons for removal, degradation, and disposal of organelles. In order to test whether ciliary neurotrophic factor (CNTF), which is present at high levels in the Schwann cell cytoplasm, is involved in the maintenance of these structures, we have examined lumbar ventral root nerve fibers of alpha‐motor neurons by electron microscopy in 3‐ and 9‐month‐old Cntf null (−/−) mutant mice. Nerve fibers and nodes of Ranvier in 3‐month‐old Cntf−/− mutants appeared morphologically normal, except that ASNs were more voluminous in the mutants than in wild‐type control animals at this age. In 9‐month‐old Cntf−/− animals, morphological changes, such as reduction in nerve fiber and axon diameter, myelin sheath disruption, and loss of ASNs at nodes of Ranvier, were observed. These findings suggest that endogenous CNTF, in addition to its role in promoting motor neuron survival and regeneration, is needed for long‐term maintenance of alpha‐motor nerve fibers. The premature loss of paranodal ASNs in animals lacking CNTF, which seems to be a defect related to a disturbed interaction in the nodal region between the axon and its myelinating Schwann cells, could impede the maintenance of a normal milieu in the motor axon, preceding more general neuronal damage. GLIA 42:340–349, 2003. © 2003 Wiley‐Liss, Inc.
Bibliography:	istex:1B7ABFDD825CBFE1001D06359187BD8B20D0831C ArticleID:GLIA10221 Handlaren Hjalmar Svenssons Forskningsfond Deutsche Forschungsgemeinschaft ark:/67375/WNG-BCM5W28S-L Swedish Medical Research Council ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2
ISSN:	0894-1491 1098-1136
DOI:	10.1002/glia.10221