Changes in slow axonal transport of tubulin induced by local application of colchicine to rabbit vagus nerve

Archer, D. R.; Dahlin, Lars B.; McLean, W. Graham

doi:10.1111/j.1748-1716.1994.tb09659.x

Cited by 7 publications

(2 citation statements)

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“…Colchicine was used at final concentrations ranging from 10 µM to 2 mM. This is lower than what has been shown to reversibly inhibit axonal transport without toxic effects and without influencing membrane potentials (Fitzgerald et al, 1984;Tiedt et al, 1977;Archer et al, 1994). By using 2 mM colchicine, a strong induction of GAP-43 and ␣-tubulin mRNA levels was obtained in the experimental and contralateral retina in all animals tested (n ϭ 6; not shown).…”

Section: Influence Of the Cytoskeleton On Gap-43 And ␣-Tubulin Gene Rmentioning

confidence: 94%

Target contact regulates GAP-43 and ?-tubulin mRNA levels in regenerating retinal ganglion cells

et al. 1998

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Axotomy of vertebrate neurons leads to the transient upregulation of GAP-43 and alpha-tubulin. In adult zebrafish retina, mRNA levels of both genes were increased in retinal ganglion cells after optic nerve lesion following a similar time course. At 5 days after crush, the mRNA level of GAP-43 was increased nearly 20 times, whereas a 6-fold increase was observed for alpha-tubulin. Subsequently, upon target reinnervation, mRNA levels of both genes were downregulated and were 2-fold higher than normal at 25 days after crush. Stretching the optic nerve that results in diffuse axonal lesions led to the expression of both genes in identical subsets of retinal ganglion cells. When regeneration was prevented by removing a piece of the optic nerve, mRNA levels remained elevated. Disruption of axonal transport by colchicine and vinblastine led to the induction of both genes in normal retina. Blocking electrical activity with tetrodotoxin had no effect. This indicates that retrogradely transported signals induced by target contact regulate GAP-43 and alpha-tubulin transcription. Furthermore, the joint regulation of GAP-43 and alpha-tubulin mRNA levels after different kinds of lesion suggests that a common pathway underlies the regulation of neuronal GAP-43 and alpha-tubulin gene expression. In contrast, distinct mechanisms may control the extent and maintenance of increased mRNA levels of these genes.

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Section: Influence Of the Cytoskeleton On Gap-43 And ␣-Tubulin Gene Rmentioning

confidence: 94%

Target contact regulates GAP-43 and ?-tubulin mRNA levels in regenerating retinal ganglion cells

et al. 1998

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“…However changes in axonal architecture were not apparent in rats with taxol-induced hyperalgesia 51 and axonal transport was not impaired in dorsal root ganglia (DRG) neurons exposed to paclitaxel in vitro at chemotherapeutic doses 28 . Reagents that disrupt the functions of microtubules such as TZT-1027 (a derivative of dolastatin) or colchicine 4,17 do not induce any morphological change in sensory nerves or hyperalgesia 47,73 . Although direct application of colchicine to the sciatic nerve blocks neurogenic plasma extravasation, changes of heat or mechanical withdrawal thresholds or the development of deafferentation-induced hyperalgesia have not been observed 33 .…”

Section: Introductionmentioning

confidence: 99%

Induction of Monocyte Chemoattractant Protein-1 (MCP-1) and Its Receptor CCR2 in Primary Sensory Neurons Contributes to Paclitaxel-Induced Peripheral Neuropathy

Zhang

Boyette-Davis

Kosturakis

et al. 2013

The Journal of Pain

129

153

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The use of paclitaxel (Taxol®), a microtubule stabilizer, for cancer treatment is often limited by its associated peripheral neuropathy (chemotherapy-induced peripheral neuropathy, CIPN) which predominantly results in sensory dysfunction including chronic pain. Here we show that paclitaxel CIPN was associated with an induction of chemokine monocyte chemoattractant protein-1 (MCP-1) and its cognate receptor CCR2 in primary sensory neurons of dorsal root ganglia (DRG). Immunostaining revealed that MCP-1 was mainly expressed in small nociceptive neurons while CCR2 was expressed in large and medium-sized myelinated neurons. Direct application of MCP-1 consistently induced intracellular calcium increases in DRG large and medium-sized but not small neurons mainly dissociated from paclitaxel- but not vehicle-treated animals. Paclitaxel also induced increased expression of MCP-1 in spinal astrocytes but no CCR2 signal was detected in spinal cord. Local blockade of MCP-1/CCR2 signaling by anti-MCP-1 antibody or CCR2 antisense oligodeoxynucleotides significantly attenuated paclitaxel CIPN phenotypes including mechanical hypersensitivity and loss of intraepidermal nerve fibers (IENFs) in hindpaw glabrous skin. These results suggest that activation of paracrine MCP-1/CCR2 signaling between DRG neurons plays a critical role in the development of paclitaxel CIPN and targeting MCP-1/CCR2 signaling could be a novel therapeutic approach.

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Taxol-induced sensory disturbance is characterized by preferential impairment of myelinated fiber function in cancer patients

Dougherty

Cata²,

Cordella

et al. 2004

Pain

341

328

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Taxol produces neuropathic pain with three distinct zones of involvement in the extremities. Most distally is an area of on-going pain and proximal to this is a zone of sensory disturbance but not overt pain. These two areas were confined in all but one case to the glabrous skin of the hands and/or feet. More proximal is an area not recognized by the patients as involved with pain or sensory disturbance yet wherein quantitative sensory tests nevertheless reveal altered sensibility. Impairment of perception to light touch, normally conveyed by myelinated fibers, was dramatically altered in all three areas, being approximately 50-fold greater than normal in areas of pain and sensory disturbance as well as in areas of skin perceived by the patients as not affected. Impairment of perception to sharpness, normally conveyed by small myelinated fibers, was most pronounced in areas of on-going pain, intermediate in areas of sensory disturbance and near baseline in more proximal skin of chemotherapy patients. In contrast to mechanical sensibility, thermal thresholds for warm and heat pain detection were normal throughout. Finally, chemotherapy patients showed paradoxical burning pain to skin cooling that was most pronounced in proximal areas of skin thought to be unaffected by the patients, intermediate in the border zone of altered sensibility and least pronounced in areas of on-going pain. These data suggest that taxol produces a neuropathy characterized by pronounced impairment of function in A-beta myelinated fibers, intermediate impairment of A-delta myelinated fibers, and a relative sparing of C-fibers.

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Changes in slow axonal transport of tubulin induced by local application of colchicine to rabbit vagus nerve

Cited by 7 publications

References 0 publications

Target contact regulates GAP-43 and ?-tubulin mRNA levels in regenerating retinal ganglion cells

Target contact regulates GAP-43 and ?-tubulin mRNA levels in regenerating retinal ganglion cells

Induction of Monocyte Chemoattractant Protein-1 (MCP-1) and Its Receptor CCR2 in Primary Sensory Neurons Contributes to Paclitaxel-Induced Peripheral Neuropathy

Taxol-induced sensory disturbance is characterized by preferential impairment of myelinated fiber function in cancer patients

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