Brain Res. 1977 Jun 10;128(2):227-42.
Inhibition of the rapid movement of optically detectable axonal particles colchicine and vinblastine.

Hammond GR, Smith RS.

The rapid saltatory motion of intra-axonal particles detected by dark-field microscopy in myelinated axons isolated from sciatic nerves of adult Xenopus laevis was inhibited by colchicine or vinblastine at a concentration of larger than or equal to 0.1 mM. Both the predominant somatopetal transport and the somatofugal transport of these round particles were inhibited. The reduction in numbers of moving particles was apparent first in the juxtanodal portions of the isolated axons within about 1 h. No particles could be detected moving by 3-5 h after application of the colchicine or vinblastine. During the phase of partial inhibition, those particles that were still progressing along the axon did so at apparently normal velocities while they were in motion, but remained stationary increasingly frequently and for progressively longer periods. Colchicine or vinblastine at a concentration of less than or equal to 10 micronM caused no observable inhibition within 4 h of application. Colchicine at a concentration of larger than or equal to 10 mM caused local accumulation of round particles, and vinblastine at a concentration of larger than or equal to 2.5 mM caused fragmentation of rod-shaped organelles, believed to be mitochondria. Electron microscopy of nerve fibers treated with 5 mM colchicine showed a progressive loss of microtubules from the axoplasm, such that approximately 70% of the microtubules had disappeared after 4h.


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Brain Res. 1977 Nov 4;136(1):31-43.
Neuronal transport in salamander nerves and its blockade by colchicine.

Holmes MJ, Turner CJ, Fried JA, Cooper E, Diamond J.

Neuronal transport and the effects of colchicine on it has been studied in salamander spinal nerves.Cholinesterase (ChE) accumulation above the cut region of a nerve at 12.5 degrees C was shown to depend upon two processes. One caused a transient increase which declined to zero by 24 h; the other was explained by axoplasmic transport. At 22 degrees C the transient change was not observed, but the rate of accumulation attributable to transport increased. The Q10 for this transport over the range 12.5 degrees C--22 degrees C is approximately three. The ChE accumulation in the sensory component of the mixed nerve was about equal to that in the motor. The rate of fast axoplasmic transport of labeled leucine was 56 mm/day at 22 degrees C; if ChE moves at the same rate, then only 7% of the total enzyme is carried by fast axoplasmic transport. The transport of ChE was reduced by at least 50% when nerves were bathed in a 75 mM solution of colchicine for 30 min; this treatment is known not to cause subsequent degeneration of these nerves. The rate of slow flow of labeled material after bathing the nerve trunk in tritiated colchicine was found to be approximately 0.5 mm/day.


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Arkh Anat Gistol Embriol. 1978 May;74(5):26-31.
[Degeneration of the laminated corpuscles (of Vater--Pacini) following colchicine application to a nerve]

[Article in Russian]

Chelyshev IuA, Vinter RI, Zefirov TL.

Laminated pacinian corpuscles from the cat mesentery have been studied morphologically and morphometrically after nerve section and colchicine application to the nerve and the results obtained are represented. Similar interventions in the nerve produce changes in the receptors resembling those of wallerian type degeneration, degeneration rate after sectioning being higher than after colchicine application. At early stages after colchicine application the internal cone and its nuclei increase in size. The data obtained suggest the nuclei of the internal cone to be under neurotrophic control of the sensory neuron that might be realized via axoplasmic transport of substances.


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J Cell Biochem. 1999 Mar 1;72(3):339-48.
Insulin-like growth factor-I-dependent stimulation of nuclear phospholipase C-beta1 activity in Swiss 3T3 cells requires an intact cytoskeleton and is paralleled by increased phosphorylation of the phospholipase.

Martelli AM, Cocco L, Bareggi R, Tabellini G, Rizzoli R, Ghibellini MD, Narducci P.

Dipartimento di Morfologia Umana Normale, Universita di Trieste, Italy. martellniv.trieste.it

Swiss 3T3 mouse fibroblasts were exposed to 10 microM colchicine to disrupt microtubules, then stimulated with insulin-like growth factor-I. Immunoprecipitation experiments showed that insulin-like growth factor-I receptor and insulin receptor substrate-1 were tyrosine phosphorylated to the same extent in both cells treated with colchicine and in those not exposed to the drug. Moreover, the activity of phosphatidylinositol 3-kinase was not affected by incubation with colchicine. While in nuclei prepared from cells not exposed to colchicine it was possible to detect an insulin-like growth factor-I-dependent increase in the mass of diacylglycerol, as well as stimulation of phospholipase C activity, no similar changes were observed in nuclei obtained from cells treated with colchicine. Activation of the nuclear phospholipase activity was paralleled by an increase of its phosphorylation. Immunofluorescent studies revealed that mitogen-activated protein kinase did not translocate towards the nucleus when the cytoskeleton was depolymerized. These results show that in Swiss 3T3 cells some as yet unknown events necessary for the insulin-like growth factor-I-dependent activation of nuclear polyphosphoinositide metabolism require the presence of an intact cytoskeleton and are situated down-stream the activation of insulin receptor substrate-1 and phosphatidylinositol 3-kinase. Activation of nuclear phospholipase C-beta1 might be linked to its phosphorylation and translocation of mitogen-activated protein kinase to the nucleus.


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