Peripheral nerve structures of experimental diabetes rats and the effect of insulin treatment.

Yagihashi, Soroku; Kudo, Kozaburo; Nishihira, Morimi

doi:10.1620/tjem.127.35

Cited by 35 publications

(20 citation statements)

References 24 publications

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“…However, it is possible that the failure of sodium nitroprusside or L-arginine completely to restore nerve LDF re¯ects an acutely irreversible modi®cation to the structure of the vasa nervorum which limited vasodilatation. Micro-vascular abnormalities such as increased basement membrane thickening and reduced endoneurial capillary density are clearly observed in the vasa nervorum of experimentally diabetic rats (Yagihashi et al, 1979;Powell et al, 1980;Cameron et al, 1991).…”

Section: Discussionmentioning

confidence: 99%

Aminoguanidine‐effects on endoneurial vasoactive nitric oxide and on motor nerve conduction velocity in control and streptozotocin‐diabetic rats

Dewhurst

Omawari

Tomlinson

1997

British J Pharmacology

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1 The e ects of aminoguanidine (AG) treatment on reductions in motor nerve conduction velocity (MNCV) and sciatic nerve blood¯ow, indexed by laser Doppler¯ux (LDF), were investigated in rats with experimental diabetes (streptozotocin-induced; 8 ± 10 weeks duration). The contribution of endoneurial vasoactive nitric oxide to the LDF of these animals was also investigated by the direct micro-injection of N G -nitro-L-arginine methyl ester (L-NAME; 1 nmol in 1 ml), followed by L-arginine (100 nmol in 1 ml), into the sciatic nerve endoneurium. 2 The MNCV (m s 71 , mean+1 s.d.) of diabetic rats (38.2+1.5) was lower (P50.01) than that of agematched controls (47.2+4.2). AG treatment (50 mg kg 71 day 71 , i.p.) attenuated the diabetes-induced de®cits in MNCV (43.4+5.9; P50.01), but had no e ect in controls (48.8+3.8) or, if administered via drinking water (1 g l 71 ), diabetics (37.4+4.1). 3 L-NAME markedly reduced the resting LDF (arbitrary units; mean+s.e.mean) of controls (209+13 to 120+18; P50.005), an e ect reversed by subsequent L-arginine (to 206+27). In diabetic rats the LDF reduction following L-NAME was much smaller (111+11 to 84+6; P50.05), but the change with Larginine was signi®cantly increased (to 145+12; P50.001). 4 AG treatment increased the resting LDF of control (265+34) and diabetic rats (133+14 for daily injection and 119+13 for drinking water). The responses to L-NAME and L-arginine were not changed markedly by AG treatment. However, L-arginine appeared to be less e ective. 5 In conclusion, these data suggest that AG treatment may a ect nitric oxide production in the vasa nervorum of peripheral nerves. However, the e ects of AG-treatment are not consistent with the prevention of a diabetes-associated reduction in endoneurial nitric oxide production. The mechanisms by which AG attenuates nerve conduction slowing in streptozotocin-diabetic rats therefore remain unclear.

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Section: Discussionmentioning

confidence: 99%

Aminoguanidine‐effects on endoneurial vasoactive nitric oxide and on motor nerve conduction velocity in control and streptozotocin‐diabetic rats

Dewhurst

Omawari

Tomlinson

1997

British J Pharmacology

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“…Injection of a single dose of streptozotocin caused rapid induction of hyperglycemia, and it mimicks type 1 diabetes mellitus [17,18]. Soon after the initial development of the streptozotocin-induced diabetes mellitus model, investigators recognized that the pathological changes in the peripheral nerves of these rats mirrored what has been seen in patients with DPN; they exhibited axonal atrophy, axonal degeneration, and demyelination [19][20][21]. These findings, however, were not very consistent across different models, and only a careful study was able demonstrate that streptozotocin-induced diabetic rats had distal axonal degeneration similar to human DPN, in which the degeneration starts in the most distal nerves in a "dying-back" fashion [22].…”

Section: Diabetic Neuropathymentioning

confidence: 99%

Animal Models of Peripheral Neuropathies

Höke

2012

Neurotherapeutics

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Peripheral neuropathies are common neurological diseases, and various animal models have been developed to study disease pathogenesis and test potential therapeutic drugs. Three commonly studied disease models with huge public health impact are diabetic peripheral neuropathy, chemotherapy-induced peripheral neuropathy, and human immunodeficiency virus-associated sensory neuropathies. A common theme in these animal models is the comprehensive use of pathological, electrophysiological, and behavioral outcome measures that mimic the human disease.

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“…Abnormalities of both Schwann cells and axon have been described. These were considered to be secondary alter ations due to a metabolic abnormality [12], The presence of dense bodies in the nerve terminals of diabetics, as demonstrated in our specimens, has not been described so far. These formations could be recognized among enlarged or distorted mitochondria and may be the result of late-stage mitochondrial degeneration in the context of axonal degen eration.…”

Section: Discussionmentioning

confidence: 49%

Electron-Microscopic Study of Iris Nerves and Muscles in Diabetes

et al. 1985

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The ultrastructure of the iris muscles and innervating nerves in patients with diabetes mellitus and approximately age-matched controls was examined by electron-microscopy. The specimens were obtained during cataract surgery. There were definite histopathological alterations at the nerve terminal innervating the dilator muscle, e. g. the presence of mitochondrial abnormalities, dense bodies and lamellar structures. No change was noted at the nerve terminal to the sphincter muscle. Moderate involvement of the muscle, especially at the sphincter, was observed in the specimens of diabetics. The control specimens had no change at the nerve terminals, while moderate change was observed at the sphincter muscle. Therefore, the change in the sphincter seen in the specimens of diabetics seemed to be mainly the result of the aging process, though the existence of early sympathetic neuropathy was confirmed.

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Peripheral nerve structures of experimental diabetes rats and the effect of insulin treatment.

Cited by 35 publications

References 24 publications

Aminoguanidine‐effects on endoneurial vasoactive nitric oxide and on motor nerve conduction velocity in control and streptozotocin‐diabetic rats

Aminoguanidine‐effects on endoneurial vasoactive nitric oxide and on motor nerve conduction velocity in control and streptozotocin‐diabetic rats

Animal Models of Peripheral Neuropathies

Electron-Microscopic Study of Iris Nerves and Muscles in Diabetes

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