Source:http://linkedlifedata.com/resource/pubmed/id/10366605
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
|
pubmed:dateCreated |
1999-6-28
|
pubmed:abstractText |
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 degrees C. At 25 degrees 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 degrees C the CAPs were minimal at 2 d. When the temperature of wild-type nerves was raised to 37 degrees C after 24-72 hr at 25 degrees C, degeneration occurred within the subsequent 24 hr. Wld nerves, too, were preserved longer at 25 degrees C but, on return to 37 degrees 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 microM 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.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Jun
|
pubmed:issn |
1529-2401
|
pubmed:author | |
pubmed:issnType |
Electronic
|
pubmed:day |
15
|
pubmed:volume |
19
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
4718-26
|
pubmed:dateRevised |
2007-11-14
|
pubmed:meshHeading |
pubmed-meshheading:10366605-Animals,
pubmed-meshheading:10366605-Axons,
pubmed-meshheading:10366605-Axotomy,
pubmed-meshheading:10366605-Body Temperature,
pubmed-meshheading:10366605-Calcium,
pubmed-meshheading:10366605-Mice,
pubmed-meshheading:10366605-Mice, Inbred C57BL,
pubmed-meshheading:10366605-Sciatic Nerve,
pubmed-meshheading:10366605-Time Factors,
pubmed-meshheading:10366605-Wallerian Degeneration
|
pubmed:year |
1999
|
pubmed:articleTitle |
Temperature modulation reveals three distinct stages of Wallerian degeneration.
|
pubmed:affiliation |
Department of Neurology, Johns Hopkins Hospital, Baltimore, Maryland 21287, USA.
|
pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.
|