Abnormal axonal inward rectification in diabetic neuropathy

Horn, Sabine; Quasthoff, Stefan; Grafe, Peter; Bostock, Hugh; Renner, R; Schrank, Berthold

doi:10.1002/mus.880191002

Cited by 84 publications

(64 citation statements)

References 31 publications

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“…A decrease in I h has been inferred in patients with diabetic neuropathy (Horn et al, 1996) and in an animal model of diabetic neuropathy (Yang et al, 2001). Our observed increase in activity-dependent slowing would be consistent with a decrease in the I h current.…”

Section: Enhanced Activity-dependent Slowing Of Uninjured C Fibers Afsupporting

confidence: 87%

Activity-dependent slowing of conduction velocity in uninjured L4 C fibers increases after an L5 spinal nerve injury in the rat

Shim

Ringkamp

Lambrinos

et al. 2007

Pain

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Growing evidence suggests that uninjured afferents may play an important role in neuropathic pain following nerve injury. The excitability of nociceptive neurons in the L4 spinal nerve appears to be enhanced following an injury to the adjacent L5 spinal nerve. In this study, we investigated whether the action-potential conduction properties of unlesioned, unmyelinated fibers are also altered. A teased-fiber technique was used to record from single C fibers from the L4 spinal nerve of the rat in vitro. Repeated electrical stimulation of the tibial nerve was used to investigate activity-dependent slowing of conduction velocity. Twin pulse stimulation at a 50 ms interpulse interval allowed investigation of supranormal conduction velocity. Blinded experiments were performed 8-10 days after sham surgery and after an L5 spinal nerve ligation (L5 SNL). Activity-dependent slowing revealed two populations of C fibers, a "nociceptor" population with a large degree of activitydependent slowing and a "non-nociceptor" population with a smaller degree of activity-dependent slowing. Both populations showed enhanced activity-dependent slowing of conduction velocity and enhanced supranormal conduction velocities in lesioned animals compared to sham animals. Activity-dependent slowing was also enhanced after an L5 SNL in the mouse. These alterations in conduction velocity may reflect changes in expression of ion channels responsible for the membrane excitability. These data provide additional evidence that a nerve injury leads to persistent alterations in the properties of adjacent uninjured, unmyelinated fibers.

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Section: Enhanced Activity-dependent Slowing Of Uninjured C Fibers Afsupporting

confidence: 87%

Activity-dependent slowing of conduction velocity in uninjured L4 C fibers increases after an L5 spinal nerve injury in the rat

Shim

Ringkamp

Lambrinos

et al. 2007

Pain

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show abstract

“…Recent data from peripheral nerves in human diabetic neuropathy indicate that axonal inward rectification might be diminished [8]. The abnormalities in diabetic patients were positively correlated with the age of patients and having neuropathy [8]. Using a similar technique on peripheral nerves in STZ-induced diabetic rats, another study also recorded a decrease in inward rectification that was reversed by an aldose reductase inhibitor treatment [9].…”

Section: Na and K Conductances Are Impaired In Early Animal Diabetesmentioning

confidence: 96%

“…Clinical studies using the threshold electrotonus technique have provided evidence that I h also occurs in human axons in situ [49], and that its effects on excitability are more pronounced in sensory than motor axons [50]. Recent data from peripheral nerves in human diabetic neuropathy indicate that axonal inward rectification might be diminished [8]. The abnormalities in diabetic patients were positively correlated with the age of patients and having neuropathy [8].…”

Section: Na and K Conductances Are Impaired In Early Animal Diabetesmentioning

confidence: 99%

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Intra-axonal recording from large sensory myelinated axons: Demonstration of impaired membrane conductances in early experimental diabetes

Križ

Padjen

2003

Diabetologia

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Aim/hypothesis. Diabetic neuropathy is accompanied by a range of positive (paresthaesia, dysesthaesia, pain) and negative (hypesthaesia, anesthaesia) neurological symptoms suggesting widespread alterations in axonal excitability. The nature and the mechanisms underlying these alterations in axonal excitability are not well understood. The aim of this study was to examine the extent of changes in membrane properties of an identified neuronal structure -the large myelinated sensory axons in early experimental diabetes in rats. Methods. Intra-axonal microelectrode recordings from large sensory myelinated axons from the isolated sural nerve in short-term streptozotocin-induced diabetic rats were used to study membrane properties using standard current-clamp technique.Results. In addition to decreased conduction velocity we found several differences in physiological properties of sensory axons from diabetic rats: decreased resting membrane potential, decreased single action potential amplitude associated with slower rate of rise and decrease in inward rectification associated with slight alteration in outwardly rectifying conductances indicating impaired potassium conductances. Conclusion/Interpretation. These results extend previous indirect evidence that potassium and sodium ionic conductances, most notably the inward rectifier (IR, I h ), are altered in large sensory axons of diabetic rats. . The pathogenesis of diabetic neuropathies and consequently their treatment remain elusive, in spite of a number of hypotheses advanced in the past decades. These hypotheses deal with several major areas, such as metabolic, ischaemia and oxidative stress, non-specific glycosylation, and disturbances in trophic factors [1,2,3,4]. The histopathological findings of advanced diabetic neuropathy (DN) are characterized by axonal degeneration, demyelination and atrophy that are associated with highly diverse disturbances of peripheral nerve function [2,5,6]. Different positive and negative neurological signs associated with DN suggest modification in axonal membrane excitability. Indeed, one of the earliest detectable physical signs of early DN is a decrease in conduction velocity as signsThe peripheral neuropathy associated with diabetes is one of the most common polyneuropathies, and at least 50% of diabetic patients will develop a form of

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“…Puls elektromanyetik alan tedavisinin, nöronların depolarize, repolarize, hiperpolarize olmasını sağlayan, aşırı derecede düşük frekanslı kuasirektanguler akım-ların oluşumunu uyararak, sodyum akışı üzerinden aksiyon potansiyelinin azalmasını veya durdurulmasını sağlayarak etkili olduğu bildirilmektedir. [18][19][20] Rasgele plasebo kontrollü çalışmamızda, semptomatik DPN tedavisinde PEMF'in nöropati semptomlarını azaltmada ne kadar etkili olduğu araştırıldı. Tedavi grubundaki tüm hastaların ayaklarına PEMF tedavisi on ardışık gün ve günde 1 saat olmak üzere uygulandı.…”

Section: Discussionunclassified

The Effects Of Pulsed Electromagnetic Field Treatment In Pain Due To Diabetic Polyneuropathy

Fezyioğlu¹,

Özdemir²,

Güldiken³

et al. 2009

TUTFD

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Objectives: Diabetic polyneuropathy is the most common and disabled complication of diabetes mellitus. Pharmacological treatment of diabetic neuropathy is limited because of the side efects of the drugs, used in the treatment of diabetic neuropthy. Alternative treatments are also used in diabetic neuropathy. Systemic side effects of non-pharmacological treatment modalities are rare. We evaluated the value of pulsed electromagnetic field treatment in patients with pain due to diabetic polyneuropathy. Patients and Methods:Symptomatic 95 patients were included in the study, and from these patients, 25 patients were randomized in pulsed electromagnetic field treatment group and 25 patients were randomized in placebo group. Pulsed electromagnetic field device was applied over both feet of the patients for one hour a day (during 10 days). Visual analog scale and neuropathic pain scale of all patients were performed before and after treatment and 6th week. Electroneuromyography was also performed before treatment and 6th week.Results: Improvement of pain determined by visual analog scale was 53% after treatment and 67% six weeks later. The improvement of visual analog scale scores were statistically significant in study group when compared with control subjects. Conclusion:The pulsed electromagnetic field may be an alternative treatment modality in diabetic patients with neuropathic pain.

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Abnormal axonal inward rectification in diabetic neuropathy

Cited by 84 publications

References 31 publications

Activity-dependent slowing of conduction velocity in uninjured L4 C fibers increases after an L5 spinal nerve injury in the rat

Activity-dependent slowing of conduction velocity in uninjured L4 C fibers increases after an L5 spinal nerve injury in the rat

Intra-axonal recording from large sensory myelinated axons: Demonstration of impaired membrane conductances in early experimental diabetes

The Effects Of Pulsed Electromagnetic Field Treatment In Pain Due To Diabetic Polyneuropathy

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