Elsevier

Brain Research Bulletin

Volume 49, Issue 6, August 1999, Pages 419-427
Brain Research Bulletin

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Cited by (24)

  • CX3CL1-mediated macrophage activation contributed to paclitaxel-induced DRG neuronal apoptosis and painful peripheral neuropathy

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    Although it is generally accepted that paclitaxel impairs axoplasmic transport by binding to the β-tubulin of microtubule and thereby induces progressive dying-back of axonopathy with subsequent painful peripheral neuropathy (Jaggi and Singh, 2012; Polomano et al., 2001), a growing body of evidence has supported that peripheral neuropathy might not be secondary to the disruption of axoplasmic transport. For example, it has been reported that disruption of axonal transport by eribulin does not lead to peripheral neuropathy (Wozniak et al., 2011) and development of mechanical allodynia (Colburn and DeLeo, 1999). Jin also reported that acetyl-l-carnitine inhibited paclitaxel-evoked pain without protective effect on the degeneration of terminal fibers (Jin et al., 2008).

  • Accuracy of regenerating motor neurons: Influence of diffusion in denervated nerve

    2014, Neuroscience
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    A small sheet of parafilm (Pechiney, Chicago, IL, USA) was placed under the exposed terminal muscle branch, and then a gelfoam pledget (Pfizer, New york, NY, USA) soaked in 25 mM colchicine (C9754, Sigma–Aldrich, St. Louis, MO, USA, dissolved in normal saline) was applied to the muscle branch for 15 min. The dose and time of colchicine application was based on previous studies in the literature for rat nerves (Colburn and DeLeo, 1999; Mader et al., 2004), and the effectiveness of this approach was verified with small pilot studies (data not shown). After removing the gelfoam, the application zone was rinsed with saline and the site closed.

  • Fenbendazole improves pathological and functional recovery following traumatic spinal cord injury

    2014, Neuroscience
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    By potentially interfering with axonal transport, FBZ could also impair axonal regeneration and sprouting. Another microtubule disrupting agent, colchicine, can cause activation of astrocytes and microglia (Colburn and DeLeo, 1999), and also affect macrophages, neutrophils and endothelial cells (Crittenden et al., 2012). Following transient spinal cord ischemia in rabbits, the combination of chloroquine and colchicine decreased the numbers of mononuclear phagocytes within the damaged spinal cord, increased survival of motor neurons, and improved functional outcomes (Giulian and Robertson, 1990).

  • Disruption of fast axonal transport in the rat induces behavioral changes consistent with neuropathic pain

    2013, Journal of Pain
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    This is the first demonstration of distal mechanical hypersensitivity following the local application of a low dose of vinblastine to the sciatic nerve, the pattern of which was comparable to the neuritis model (see also8,25). A small number of studies have examined pain behavior following the local application of colchicine to the sciatic nerve but none demonstrated mechanical or heat hypersensitivities.14,36,58 The lack of effect in these studies was most likely related to the dose of colchicine tested (5 and >25 mM).

  • The double crush syndrome revisited - A Delphi study to reveal current expert views on mechanisms underlying dual nerve disorders

    2011, Manual Therapy
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    A combination of mechanisms may also counter the criticism that impaired axonal transport by itself is insufficient to explain dual nerve disorders. Axonal transport obstruction has been shown to lead to morphological changes of the cell body and to glial cell activation in the spinal cord (Colburn and DeLeo, 1999), which may explain the coexistence of ulnar and median neuropathies. Whereas the expert retention rate was high with only one expert’s opinion lost in round three, a possible limitation of this study is the low participation rate among basic scientists (19%).

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