Ganglioside Treatment Modifies Abnormal Elemental Composition in Peripheral Nerve Myelinated Axons of Experimentally Diabetic Rats

LoPachin, Richard M.; Castiglia, Carolyn M.; Saubermann, Albert J.; Eichberg, Joseph

doi:10.1111/j.1471-4159.1993.tb03175.x

Cited by 9 publications

(3 citation statements)

References 52 publications

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“…Paranodal and nodal regions were also identified and analyzed, although the small number of respective analyses precluded statistical evaluation (LoPachin et a!., 1993). The mitochondrial compartment has been identified according to both gross structural (e.g., size, shape, and orientation) and functional (e.g., differential response to injury, Ca sequestration) criteria and is designated as "mitochondrial area" (LoPachin et a!., 1988(LoPachin et a!., , 1992a(LoPachin et a!., , 1993. Mitochondrial data presented here represent analyses pooled from large and medium fibers.…”

Section: Epmamentioning

confidence: 99%

Mechanisms of Injury‐Induced Calcium Entry into Peripheral Nerve Myelinated Axons: Role of Reverse Sodium‐Calcium Exchange

Lehning

Doshi

Isaksson

et al. 1996

Journal of Neurochemistry

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Section: Epmamentioning

confidence: 99%

Mechanisms of Injury‐Induced Calcium Entry into Peripheral Nerve Myelinated Axons: Role of Reverse Sodium‐Calcium Exchange

Lehning

Doshi

Isaksson

et al. 1996

Journal of Neurochemistry

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“…Purified preparations of individual or mixed gangliosides were initially shown to have both survival and growth-promoting effects on neurons in vitro and to enhance peripheral nerve regeneration after injury in vivo [173]. A number of subsequent studies reported that ganglioside treatment also prevented a number of biochemical, functional and structural disorders in the nerves of diabetic rodents [174][175][176][177][178][179][180][181][182][183][184][185]. The mechanisms by which ganglioside therapy protects nerves from diabetes have not been fully established, although some intriguing studies reported that they modulate the efficacy of growth factor receptors and ion channels [186][187][188].…”

Section: Gangliosidesmentioning

confidence: 98%

Growth Factors as Therapeutics for Diabetic Neuropathy

Calcutt¹,

Jolivalt²,

Fernyhough³

2008

CDT

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There has been a rapid growth in appreciation of the diverse array of neurotrophic factors, growth factors and other biological molecules that have the capacity to support adult neurons and direct reparative processes after injury to the nervous system. Understanding the mechanisms by which these factors operate offers the opportunity to use either the factors themselves or other agents that manipulate relevant signal transduction pathways as therapeutics for a wide range of neurodegenerative diseases, including diabetic neuropathy. In this review, we aim to summarize current knowledge of the extent to which loss of neurotrophic support contributes to the pathogenesis of diabetic neuropathy, present pre-clinical evidence that supports the potential efficacy of growth factors or their mimetics against indices of diabetic neuropathy and highlight the emerging approaches to manipulating neuronal support mechanisms that show potential for translation to clinical use. Recent advances in directly assessing the progression of nerve damage in diabetic patients will hopefully facilitate renewed clinical evaluation of treatments for degenerative diabetic neuropathy and provide the framework for advancing the potential of growth factors as a therapy for this widespread and currently untreatable condition.

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“…Whereas this might appear inconsistent with proposed pump involvement, control intraaxonal Na levels were also maintained after ganglioside stimulation of axolemmal Na~,K~-ATPase activity (LoPachin et a!., 1993). As we have suggested, the stability of total elemental Na concentrations during Na±,K + -ATPase stimulation probably represents regulatory homeostatic adjustments by normal peripheral nerve axons and glia (for additional discussion, see LoPachin et al, 1993).…”

Section: ~0mentioning

confidence: 99%

Rubidium Uptake and Accumulation in Peripheral Myelinated Internodal Axons and Schwann Cells

Lehning

Gaughan

Eichberg

et al. 1997

Journal of Neurochemistry

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To study mechanisms of K+ transport in peripheral nerve, uptake of rubidium (Rb+), a K+ tracer, was characterized in rat tibial nerve myelinated axons and glia. Isolated nerve segments were perfused with zero‐K+ Ringer's solutions containing Rb+ (1–20 mM) and x‐ray microanalysis was used to measure water content and concentrations of Rb, Na, K, and Cl in internodal axoplasm, mitochondria, and Schwann cell cytoplasm and myelin. Both axons and Schwann cells were capable of removing extracellular Rb+ (Rb+o) and exchanging it for internal K+. Uptake into axoplasm, Schwann cytoplasm, and myelin was a saturable process over the 1–10 mM Rb+o concentration range, although corresponding axoplasmic uptake rates were higher than respective glial velocities. Mitochondrial accumulation was a linear function of axoplasmic Rb+ concentrations, which suggests involvement of a nonenzymatic process. At 20 mM Rb+o, a differential stimulatory response was observed; i.e., axoplasmic Rb+ uptake velocities increased more than fivefold relative to the 10 mM rate, and glial cytoplasmic uptake rose almost threefold. Finally, Rb+o uptake rate into axons and glia was completely inhibited by ouabain (2–4 mM) exposure or incubation at 4°C. These results suggest that Rb+ uptake into peripheral nerve internodal axons and Schwann cells is mediated by Na+,K+‐ATPase activity and implicate the presence of axonal‐ and glial‐specific Na+ pump isozymes.

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Ganglioside Treatment Modifies Abnormal Elemental Composition in Peripheral Nerve Myelinated Axons of Experimentally Diabetic Rats

Cited by 9 publications

References 52 publications

Mechanisms of Injury‐Induced Calcium Entry into Peripheral Nerve Myelinated Axons: Role of Reverse Sodium‐Calcium Exchange

Mechanisms of Injury‐Induced Calcium Entry into Peripheral Nerve Myelinated Axons: Role of Reverse Sodium‐Calcium Exchange

Growth Factors as Therapeutics for Diabetic Neuropathy

Rubidium Uptake and Accumulation in Peripheral Myelinated Internodal Axons and Schwann Cells

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