WWW.JNEUROSCI.ORG
-
The Journal of Neuroscience Synaptic Systems Antibody Company
QUICK SEARCH:   [advanced]


     
-


HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit an eLetter
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (15)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Tsao, J. W.
Right arrow Articles by Griffin, J. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tsao, J. W.
Right arrow Articles by Griffin, J. W.

 Previous Article  |  Next Article 

The Journal of Neuroscience, June 15, 1999, 19(12):4718-4726

Temperature Modulation Reveals Three Distinct Stages of Wallerian Degeneration

Jack W. Tsao , Edwin B. George, and John W. Griffin

Department of Neurology, Johns Hopkins Hospital, Baltimore, Maryland 21287

After peripheral nerve transection, axons distal to the cut site rapidly degenerate, a process termed Wallerian degeneration. In wild-type mice the compound action potential (CAP) disappears by 3 d. Previous studies have demonstrated that cold temperatures and lower extracellular calcium ion (Ca2+) concentrations can slow the rate of Wallerian degeneration. We have incubated isolated sciatic nerve segments from wild-type and C57BL/Wld mice (which carry a gene slowing Wallerian degeneration) in vitro at 25 and 37°C. At 25°C we found that the degeneration rate of wild-type axons was slowed dramatically, with the CAP preserved up to 7 d post-transection. In contrast, at 37°C the CAPs were minimal at 2 d. When the temperature of wild-type nerves was raised to 37°C after 24-72 hr at 25°C, degeneration occurred within the subsequent 24 hr. Wld nerves, too, were preserved longer at 25°C but, on return to 37°C, degenerated promptly. Cooling the nerve within 12 hr after axotomy enhanced axonal preservation. Neither wild-type nor Wld nerves showed different degeneration rates when they were incubated with 250 µM or 5 or 10 mM extracellular Ca2+ for 1-2 d, suggesting that an abrupt increase in intracellular Ca2+ occurs at the time of axonal destruction. Wallerian degeneration, thus, appears to progress through three distinct stages. Initiation occurs at the time of injury with subsequent temperature-dependent and -independent phases. Nerves appear to remain intact and are able to exclude Ca2+ from entering until an as yet unknown process finally increases axolemmal permeability.

Key words: Wallerian degeneration; temperature; C57BL/Wld mice; axonal degeneration; calcium; in vitro

Copyright © 1999 Society for Neuroscience  0270-6474/99/19124718-09$05.00/0


This article has been cited by other articles:


Home page
 J Bone Joint Surg BrHome page
S. Hall
The response to injury in the peripheral nervous system
J Bone Joint Surg Br, October 1, 2005; 87-B(10): 1309 - 1319.
[Full Text] [PDF]

Home page
 IOVSHome page
N. Goldenberg-Cohen, Y. Guo, F. Margolis, Y. Cohen, N. R. Miller, and S. L. Bernstein
Oligodendrocyte Dysfunction after Induction of Experimental Anterior Optic Nerve Ischemia
Invest. Ophthalmol. Vis. Sci., August 1, 2005; 46(8): 2716 - 2725.
[Abstract] [Full Text] [PDF]


-

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help
-
Copyright 2008 by Society for Neuroscience ONLINE ISSN: 1529-2401
-