Linked Life Data

2441026

Source:http://linkedlifedata.com/resource/pubmed/id/2441026

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1987-8-31
pubmed:abstractText
Using the frog sciatic nerve as an in vitro model system, the effects of 10(-5) M nocodazole, an antimitotic drug, on rapid axoplasmic transport were quantified and tested for reversibility. After pulse-labeling the 8th dorsal root ganglia with [3H]leucine, the nerves were incubated for 4.5 to 9 hr at 25 degrees C. Transport velocities and amounts of transported material were determined from the distribution of radioactively labeled proteins. One nerve per animal served as a control. Before ganglia labeling, the nerves were preincubated for 1 or 15 hr in 10(-5) M nocodazole, respectively. In one set of experiments, the nerves were preincubated in nocodazole for 6 hr washed for 1.5 hr and further treated in Ringer's solution to test for reversibility. We found that nocodazole did not affect the maximal transport velocity under any of the conditions tested. The amounts of rapidly transported material were reduced to 60% of controls after 1 hr of pretreatment with nocodazole, and to 30% after 6 to 15 hr of pretreatment. There was no indication for a reversibility of these effects. We conclude that 10(-5) M nocodazole shows maximal effects on rapid axoplasmic transport only if given several hours before protein synthesis, and that it reduces the capacity of rapid axoplasmic transport without affecting transport velocity. These effects are not reversible during the survival time of the in vitro preparation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
242
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
277-83
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Nocodazole irreversibly reduces the capacity of rapid axoplasmic transport in vitro.
pubmed:publicationType
Journal Article