Neurotrophins and Peripheral Neuropathy

The most common form of peripheral neuropathy is that associated with diabetes mellitus. In rodent models of diabetes there are expression deficits in nerve growth factor (NGF) and in its high-affinity receptor, trkA, leading to decreased retrograde axonal transport of NGF and decreased support of N...

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Bibliographic Details
Published in:Philosophical transactions of the Royal Society of London. Series B. Biological sciences 1996-03, Vol.351 (1338), p.455-462
Main Authors: Tomlinson, D. R., Fernyhough, P., Diemel, L. T.
Format: Article
Language:English
Subjects:
Animals
Diabetes
Diabetes complications
Diabetes mellitus
Diabetic neuropathies
Diabetic Neuropathies - drug therapy
Diabetic Neuropathies - etiology
Gene Expression Regulation
Humans
Insulin
Insulin - pharmacology
Messenger RNA
Nerve Growth Factors - pharmacology
Nerve Growth Factors - physiology
Nerves
Neurons
Neurotrophin 3
Proto-Oncogene Proteins - physiology
Rats
Receptor Protein-Tyrosine Kinases - physiology
Receptor, trkA
Receptors
Receptors, Nerve Growth Factor - physiology
Roles in the Adult
Sciatic nerve
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Summary:The most common form of peripheral neuropathy is that associated with diabetes mellitus. In rodent models of diabetes there are expression deficits in nerve growth factor (NGF) and in its high-affinity receptor, trkA, leading to decreased retrograde axonal transport of NGF and decreased support of NGF-dependent sensory neurons, with reduced expression of their neuropeptides, substance P and calcitonin gene-related peptide (CGRP). Treatment of diabetic rats with intensive insulin normalized these deficits and treatment with exogenous NGF caused dose-related increases, giving levels of NGF and neuropeptides which were greater than those of controls. Neurotrophin-3 (NT-3) mRNA was also deficient in leg muscle from diabetic rats and administration of recombinant NT-3 to diabetic rats increased the conduction velocity of sensory nerves without affecting motor conduction velocity. These findings implicate deficient neurotrophic support in diabetic neuropathy and suggest that its correction should be a paramount therapeutic target.
ISSN:0962-8436
1471-2970
DOI:10.1098/rstb.1996.0042