Impaired myelinated fiber regeneration following freeze-injury in rats with streptozotocin-induced diabetes: involvement of the polyol pathway

Love, A.; Cotter, Mary A.; Cameron, Norman E.

doi:10.1016/0006-8993(95)01070-x

Cited by 13 publications

(10 citation statements)

References 41 publications

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“…The impaired regeneration following nerve damage is in agreement with other studies on diabetic rats (Bisby 1980;Longo et al 1986;Ekström et al 1989;Love et al 1995). Prevention of regeneration deficits by a -tocopherol treatment has not previously been reported.…”

Section: Fig 3 Effects Of Diabetes Andsupporting

confidence: 82%

“…There is a reduced regenerative response to nerve damage in experimental diabetes (Bisby 1980;Longo et al 1986;Love et al 1995), and regenerative capacity is impaired in diabetic neuropathic patients (Thomas and Eliasson 1984). It is not known whether these changes depend on similar mechanisms to those responsible for reduced NCV, as opposed to other altered metabolic or neurotrophic factors (Vinik et al 1995).…”

Section: Introductionmentioning

confidence: 99%

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Effects of α-tocopherol on nerve conduction velocity and regeneration following a freeze lesion in immature diabetic rats

Love

Cotter

Cameron

1996

Naunyn-Schmiedeberg's Arch Pharmacol

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We investigated whether anti-oxidant treatment with alpha-tocopherol (1 g kg-1 day-1) could prevent the blunting of the normal maturational increase in motor and sensory nerve conduction velocity when diabetes is induced by streptozotocin in young rats. A further study in the same rats examined effects on myelinated fibre regeneration distance 14 days after a punctate sciatic nerve lesion by a liquid nitrogen cooled probe. In non-diabetic rats between 8 and 14 weeks of age, sciatic motor and saphenous sensory conduction velocity increased by approximately 28% (P < 0.001) and 21% (P < 0.001) respectively. Diabetes induced at 8 weeks blunted this maturational change by 65% for sciatic motor and almost completely for saphenous sensory fibres (P < 0.001). Treatment with alpha-tocopherol from diabetes induction totally prevented motor conduction velocity deficits (P < 0.001). For sensory saphenous nerve, conduction abnormalities were markedly attenuated (72%, P < 0.001) although a significant deficit remained compared to age-matched non-diabetic rats (P < 0.01). Sciatic nerve myelinated fibre regeneration distance, 14 days post lesion, was 15% reduced (P < 0.001) by untreated diabetes. However, in diabetic rats treated with alpha-tocopherol, regeneration distance was significantly improved (P < 0.001), being within the non-diabetic range. Thus, the data highlight the importance of reactive oxygen species in the aetiology of impaired nerve maturation and regeneration in experimental diabetes and indirectly support the view that anti-oxidant treatment could have a therapeutic role in patients.

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Section: Fig 3 Effects Of Diabetes Andsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Effects of α-tocopherol on nerve conduction velocity and regeneration following a freeze lesion in immature diabetic rats

Love

Cotter

Cameron

1996

Naunyn-Schmiedeberg's Arch Pharmacol

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“…A few have been shown to have some reversing activity. N-acetylcysteine, a hydrophilic antioxidant and sulfydryl donor, has been shown to reverse NCV and nerve blood flow after 1 month of untreated diabetes and improved sciatic nerve mylenated fiber regeneration (58). A neurotrophic peptide of prosaposin proved efficacious in preventing onset of large and small fiber dysfunction and thermal hypoalgesia in diabetic rats (50).…”

Section: Discussionmentioning

confidence: 99%

Erythropoietin both protects from and reverses experimental diabetic neuropathy

Bianchi

Büyükakıllı

Brines

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

238

179

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Tail-nerve conduction velocities (NCV) was assessed at 5 and 11 weeks for the preventive and therapeutic schedule, respectively. Compared to nondiabetic rats, NCV was 20% lower after 5 weeks in the STZ group, and this decrease was attenuated 50% by rhEPO. Furthermore, the reduction of Na ؉ ,K ؉ -ATPase activity of diabetic nerves (by 55%) was limited to 24% in the rhEPO-treated group. In the therapeutic schedule, NCV was reduced by 50% after 11 weeks but by only 23% in the rhEPO-treated group. rhEPO treatment attenuated the decrease in compound muscle action potential in diabetic rats. In addition, rhEPO treatment was associated with a preservation of footpad cutaneous innervation, as assessed by protein gene product 9.5 immunostaining. Diabetic rats developed alterations in mechanical and thermal nociception, which were partially reversed by rhEPO given either in a preventative or therapeutic manner. These observations suggest that administration of rhEPO or its analogues may be useful in the treatment of diabetic neuropathy.

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“…Conduction velocities of regenerating axons also reflect their maturity through myelination and rise in girth ( Terada et al, 1996 ) . Other in vitro electrophysiological approaches are also available, such as measures of compound nerve action potentials in vitro at an array of distances along the nerve from the injury site ( Love et al, 1995 ; Maxfield et al, 1995 ) . Finally, behavioral approaches to measure the success of regeneration are important, but must take enough time to be measurable.…”

Section: Evidence For Failed Regeneration In Diabetic Peripheral Nervesmentioning

confidence: 99%

Impaired peripheral nerve regeneration in diabetes mellitus

Kennedy

Zochodne

2005

J Peripheral Nervous Sys

164

102

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Diabetes mellitus impairs peripheral nerve regeneration. Regenerative failure likely exacerbates deficits from polyneuropathy or focal neuropathies in patients who might otherwise exhibit spontaneous improvement. Some focal neuropathies, like carpal tunnel syndrome, are common, yet render ongoing disability because of their delayed recovery. Why diabetic nerves fail to regenerate is an interesting question to consider because several mechanisms likely contribute. In this review, we examine a number of these causes. These causes include microangiopathy or disease of small blood vessels, failure to provide proper metabolic support for repair, defects in the entry and actions of inflammatory cells within the injury milieu, less robust support of axons by their Schwann cells, and lack of a full repertoire of trophic factors. A number of the mechanisms that generate neuropathy in the first place also likely contribute to failed regenerative programs, but how they do so is not clear.

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Impaired myelinated fiber regeneration following freeze-injury in rats with streptozotocin-induced diabetes: involvement of the polyol pathway

Cited by 13 publications

References 41 publications

Effects of α-tocopherol on nerve conduction velocity and regeneration following a freeze lesion in immature diabetic rats

Effects of α-tocopherol on nerve conduction velocity and regeneration following a freeze lesion in immature diabetic rats

Erythropoietin both protects from and reverses experimental diabetic neuropathy

Impaired peripheral nerve regeneration in diabetes mellitus

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