Pathology of Axonal Transport

McLean, W. Graham; Frizell, M.; Sjöstrand, Johan

doi:10.1007/978-1-4757-6740-7_3

Cited by 2 publications

(3 citation statements)

References 146 publications

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“…Microtubules are essential for axonal transport, a process known to be affected by as early as 14 days of ex-perimental diabetes [2,3]. Highly reactive lysine residues are essential for assembly of tubulin into microtubules, and their substitution prevents assembly [10,11].…”

Section: Discussionmentioning

confidence: 99%

“…The in vitro conditions of their study might permit a reversal of short-term influences on transport that would exist in vivo, but not, presumably, a reversal of non-enzymatic glycation. Tubulin glycation may, 389 however, contribute to the rather more clearly defined changes in slow transport of cytoskeletal proteins in experimental diabetes [3,13] that may be related to reduced axon diameter.…”

Section: Discussionmentioning

confidence: 99%

“…Certain aspects of axonal transport are compromised at an early stage in the diabetic rat [2,3]. Fast anterograde and retrograde axonal transport are dependent on intact microtubules [4], while slow axonal transport involves movement ofaxonal microtubules or their subunit proteins [5].…”

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confidence: 99%

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Glycation of rat sciatic nerve tubulin in experimental diabetes mellitus

et al. 1991

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Diabetic neuropathy is associated with some early defects of axonal transport in experimental animals. Axonal transport is dependent on intact microtubules, and unsubstituted lysine residues of tubulin are essential for microtubule polymerization. As lysine residues are the major target for the non-enzymatic attachment of glucose, the effect of diabetes on the extent of glycation of tubulin was investigated. There was a more than four-fold increase in the extent of glycation of tubulin in the sciatic nerve of rats with streptozotocin-induced diabetes of 2 weeks duration compared with control rats. In contrast, no such increase in glycation was observed in brain microtubule protein from diabetic rats at that stage of diabetes. Incubation of brain microtubule protein with glucose prior to in vitro polymerization showed that the early stages of glycation were not associated with inhibition of microtubule assembly. The observed glycation of peripheral nerve tubulin in early experimental diabetes may nevertheless contribute to axonal transport abnormalities through an as yet undetermined impairment of microtubule function.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Glycation of rat sciatic nerve tubulin in experimental diabetes mellitus

et al. 1991

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The neurone and its response to peripheral, nerve compression

Dahlin

Lundborg

1990

The Journal of Hand Surgery: Journal of the British Society for

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In all types of peripheral nerve injury, it is important to realize that the lesion affects one extended cell, the neurone, which extends from the central nervous system down to the target tissue in the extremity. Compression of a peripheral nerve can disturb the intraneural transport (axonal transport) of a large variety of substances. This may be followed by morphological and biochemical changes in the nerve cell body. These central changes may effect the axon as a whole and confer on the nerve an increased susceptibility to trauma. Studies concerning the reaction of neurones to compression, relevant when discussing the double crush syndrome, are reviewed.

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Pathology of Axonal Transport

Cited by 2 publications

References 146 publications

Glycation of rat sciatic nerve tubulin in experimental diabetes mellitus

Glycation of rat sciatic nerve tubulin in experimental diabetes mellitus

The neurone and its response to peripheral, nerve compression

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