The role of axonal transport and impulse conduction on the uptake and retrograde transport of nerve growth factor and bovine serum albumin in peripheral nerve

Boegman, R.J.; Riopelle, Richard J.

doi:10.1002/neu.480110508

Cited by 9 publications

(2 citation statements)

References 11 publications

(13 reference statements)

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“…Some studies report that demyelination reduces anterograde protein transport, although this effect seems to depend on the model being studied (62)(63)(64)(65)(66)(67). Vesicle trafficking and retrograde transport of certain compounds has been found to decrease with electrical inactivity (68,69). Finally, several studies have shown that demyelination or disruption of myelin composition in gene-knockout mice can lead to axon degeneration (70)(71)(72)(73)(74).…”

Section: Degenerative Changes Without Extensive Loss Of Cell Bodies Omentioning

confidence: 99%

Extensive Injury of Descending Neurons Demonstrated by Retrograde Labeling in a Virus-Induced Murine Model of Chronic Inflammatory Demyelination

Ure¹,

Rodriguez²

2000

J Neuropathol Exp Neurol

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Abstract. Persistent Theiler's virus infection of SJL/J mice was used as a model to quantitatively assess the extent of descending neuron injury by chronic inflammatory demyelination of the spinal cord. By 9 months postinfection, inflammatory demyelinating lesions were present throughout the spinal cord, affecting up to 31% of the cross-sectional area of the ventrolateral columns. Axon dropout was evident in the lesions by electron microscopy and by quantitation of axons in normalappearing white matter. Axon number in the ventrolateral columns at L1/L2 was reduced by 23% and total axon area was reduced by 37%, compared with uninfected mice. The most informative data on descending neuron injury, however, was a reduction in retrograde, Fluoro-Gold labeling. Labeling from T11/T12 of rubrospinal, reticulospinal/raphespinal, and vestibulospinal neurons was reduced by 60%, 70%, and 93%, respectively. Retrograde responses to axonal injury were observed, consisting of atrophied cell bodies, indented nuclei, and abundant lipofuscin, but cell body dropout was minimal. The number of cell bodies of vestibulospinal neurons was reduced by only 35%, whereas the number of cell bodies of rubrospinal neurons was unchanged. These results demonstrate that chronic inflammatory demyelination can severely injure axons and emphasize the need to design neuroprotective therapies in human multiple sclerosis.

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Section: Degenerative Changes Without Extensive Loss Of Cell Bodies Omentioning

confidence: 99%

Extensive Injury of Descending Neurons Demonstrated by Retrograde Labeling in a Virus-Induced Murine Model of Chronic Inflammatory Demyelination

Ure¹,

Rodriguez²

2000

J Neuropathol Exp Neurol

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“…Although this may be important in vivo, it cannot explain our findings as the serum samples were dialysed before use to remove such low molecular weight substances, and glucose was undetectable after dialysis. Albumin is taken lip and transported retrogradely in nerve axons (Gainer and Fink, 1982;Boegman and Riopelle, 1980) and is one of several proteins found within the sciatic nerve of the diabetic rat which are glycosylated (Vlassara et al, 1981). Whether the inhibitory factor is glycosylated albumin or some other related factor is still to be determined.…”

Section: Discussionmentioning

confidence: 99%

A Factor in the Serum of Diabetic Patients Inhibits Microtubule Formation

If¹,

Sj²,

Wg³

2009

Exp Clin Endocrinol Diabetes

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The effect of serum from non-diabetic patients, diabetics without neuropathy and diabetics with significant neuropathy on the ability of pig brain microtubule proteins to polymerize in vitro to microtubules was observed. The extent of polymerisation on the second and third cycles of polymerisation was significantly reduced in the presence of diabetics' serum compared with non-diabetics' serum. No significant difference between the serum samples from diabetics with and without neuropathy could be found. The finding suggests the presence of a factor in the serum of diabetics, whether or not they have neuropathy, which will impair microtubule formation in vitro.

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