Interstitial Hyperosmolarity May Cause Axis Cylinder Shrinkage in Streptozotocin Diabetic Nerve

Sugimura, Kimiya; Windebank, Anthony J.; Natarajan, Viswanathan; Lambert, Edward H.; Schmid, Harald H.O.; Dyck, Peter James

doi:10.1097/00005072-198011000-00010

Cited by 82 publications

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“…The reduction in axon circularity seen in the present study supports the observations of Sugimura et al [13]. They suggested that the cause was axonal shrinkage due to hyperosmolarity of the extracellular fluid in diabetes.…”

Section: Discussionsupporting

confidence: 92%

“…Another morphological finding, the increase in myelin area and consequent reduction in axon/myelin ra-tio in untreated diabetic rats, is in good agreement with some previous light and electron microscopic studies [4,13,19] using relatively mature animals. The cause of myelin expansion is obscure.…”

Section: Discussionsupporting

confidence: 91%

“…Axon area remained at onset levels, as did conduction velocity in untreated diabetic rats, whereas normal animals showed age-related increases in both these parameters. The retardation in axon growth is in agreement with other light and electron microscopy studies [4,13,19] using relatively mature rats, although Zemp et al [20] found that axons grew normally when diabetes was induced in very immature animals. The reason for such age-related differences is not known and requires further investigation, but paradoxically it appears that diabetes during the rapid growth phase has less effect on axons than when they are more fully developed.…”

Section: Discussionsupporting

confidence: 88%

“…Fibre diameter was estimated from fibre area as the diameter of an equivalent area circle [12]. For fibres with an area greater than 20 lxm 2, measurements were also made of axon area, myelin area, and axon circularity [13]. The fractional area of the fascicle not occupied by myelinated nerve fibres or blood vessels may be defined as the "endoneurial fraction" and was estimated using a point counting technique [4].…”

Section: Morphologymentioning

confidence: 99%

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The effects of Sorbinil on peripheral nerve conduction velocity, polyol concentrations and morphology in the streptozotocin-diabetic rat

et al. 1986

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Summary. This study examined the effects of an aldose reductase inhibitor, Sorbinil, on neuropathy over a 6-month period in streptozotocin-diabetic rats. Sorbinil treatment prevented the 10-fold increase in nerve sorbitol found with diabetes. It produced a 60% improvement in tibial nerve motor conduction velocity after 6 months. Morphometric profiles of nerves were also normalised. Axon area was reduced by 14% in untreated diabetic rats compared to age-matched controls, whereas Sorbinil-treated animals showed normal age-related axon growth. Myelin area was increased by 28% in untreated diabetic animals, but was the same as age-matched controls with Sorbinil treatment. Nerve myo-inositol levels were reduced by 45% after three months of untreated diabetes, but were normal after six months. Sorbinil treatmend tended to restore myo-inositol levels toward normal over the shorter time period. It was concluded that axon growth retardation is the most likely cause of the conduction deficit seen in longterm experimental diabetes.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 88%

Section: Morphologymentioning

confidence: 99%

See 2 more Smart Citations

The effects of Sorbinil on peripheral nerve conduction velocity, polyol concentrations and morphology in the streptozotocin-diabetic rat

et al. 1986

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“…It is unlikely to be the effect of a generalised osmotic disorder of the nerves, for example the hypertonic effect of hyperglycaemia [22,23] or sorbitol [24], because the unmyelinated nerves were not affected. Also a closer relationship between CVs and plasma glucose than with HbA1 or dW would be expected in such a situation.…”

Section: Discussionmentioning

confidence: 99%

The correlation between sensory nerve conduction velocities and three metabolic indices in rats treated with streptozotocin

Julu

1988

Diabetologia

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Summary.The fastest conduction velocities of the myelinated (A) and unmyelinated (C) sensory nerve fibres were measured in the saphenous nerves of rats made diabetic up to 5 weeks previously by injection of streptozotocin. The conduction velocity of the fastest A-alpha fibres in treated rats fell by 25% compared to control rats. The effect on the slow A-delta fibres was small but C-fibres were not affected. Levels of glycosylated haemoglobin, random plasma glucose, and the net changes in body weights were also measured. There were significant changes in these three metabolic indices among diabetic rats (t7 <0.001) and the three indices were inter-related. There was a good correlation between A-fibre conduction velocity and levels of glycosylated haemoglobin but no significant relationship between C-fibre conduction velocity and this metabolic index. A-fibre conduction velocity was statistically more correlated with levels of glycosylated haemoglobin than the other two metabolic indices (p < 0.01).Key words: Diabetes, streptozotocin, A-fibres, C-fibres, conduction velocity, glycosylated haemoglobin, random plasma glucose, body weight.It is now well established that peripheral nerve conduction velocity (CV) is slowed in experimental diabetes mellitus [1][2][3][4]. Of the various animal models used, motor nerve CV has been studied most. Data on sensory nerve CV in experimental models of diabetes include reduced sensory nerve CV in the dorsal spinal root [1], saphenous nerve [2], tibial nerve [5], sural and tibial nerves [6]. No detailed data on cutaneous nerve conduction velocity in experimental diabetes is available.It is also now generally agreed that peripheral nerve conduction abnormalities occur in diabetic peripheral neuropathy in man [7][8][9][10][11][12]. It is interesting that sensory nerves respond rather differently to treatment compared with motor nerves. For example, vibratory threshold did not improve with short-term insulin therapy and yet motor nerve CV increased [13]; sensory action potential showed no improvement with insulin treatment while motor nerve CV increased [14]; sensory nerve CV did not improve with diet treatment in Type 2 (non-insulin-dependent) diabetic patients but motor nerve CV improved and correlated well with fasting plasma glucose concentrations [15]. Improvement in both sensory nerve CV and sensory action potential only began after intensive insulin treatment for a long period [16]. This unique response of sensory nerves to the treatment of diabetes, and the fact that the symptoms of diabetic neuropathy are mainly sensory [17], calls for a more detailed study of the sensory nerves especially in experimental models of diabetes where the different classes of fibres can be sampled easily.This study was undertaken to provide some more data on cutaneous nerve CVs in streptozotocin-diabetes and to correlate these with three metabolic indices in order to throw light on the possible mechanism(s) leading to conduction abnormalities. Materials and methods Experimental animalsThirty femal...

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Thin axons relative to myelin spiral length in hereditary motor and sensory neuropathy, type I

Nukada

Dyck

Karnes

1983

Annals of Neurology

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The relationship of axonal to myelin area in semithin transverse sections of myelinated fibers obtained from sural nerves at the ankle level was morphometrically assessed using computer imaging. Ten patients with hereditary motor and sensory neuropathy, type I and 41 control subjects were examined. In large- and intermediate-diameter myelinated fibers of diseased nerves, axons were significantly attenuated relative to the amount of myelin. Using electron micrographs, a similar finding was obtained when axon area was regressed on myelin spiral length. The altered relationship was found to be greater with more severe fiber loss. These data, plus other evidence, indicate that in this disorder there is a progressive atrophy of axons, usually most severe in distal aspects of lumbosacral neurons and associated with secondary segmental demyelination and remyelination and hypertrophic neuropathy, preceding distal axonal loss. Because the process may begin in utero or in infancy, not only atrophy but also maldevelopment of axons may be involved.

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Interstitial Hyperosmolarity May Cause Axis Cylinder Shrinkage in Streptozotocin Diabetic Nerve

Cited by 82 publications

References 0 publications

The effects of Sorbinil on peripheral nerve conduction velocity, polyol concentrations and morphology in the streptozotocin-diabetic rat

The effects of Sorbinil on peripheral nerve conduction velocity, polyol concentrations and morphology in the streptozotocin-diabetic rat

The correlation between sensory nerve conduction velocities and three metabolic indices in rats treated with streptozotocin

Thin axons relative to myelin spiral length in hereditary motor and sensory neuropathy, type I

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