Peroxidative aggregation of myelin membrane proteins

Konat, G.; Gantt, G.; Gorman, Amy; Wiggins, R. C.

doi:10.1007/bf01001779

Cited by 12 publications

(6 citation statements)

References 23 publications

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“…It has also been shown that the changes observed in myelin during aging can be reproduced in in vitro oxidation experiments [68]. In vitro oxidation of isolated myelin by free radicals pro duces a decrease in the major myelin proteins [69], lead ing to the formation of molecular aggregates of these proteins. These investigators proposed that the oxidative damage could produce aggregation of PLP.…”

Section: Astrocytes and Neuronesmentioning

confidence: 90%

Thyroid Hormones and the Central Nervous System

Pasquini

Adamo²

1994

Dev Neurosci

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Thyroid hormones have a significant influence on the development and maturation of the central nervous system. Among their actions, T₃ and T₄ have effects on the differentiation of various cell types in the rat brain and cerebellum as well as on the process of myelination. Recently, several investigators have shown effects of thyroid hormones on myelin protein gene expression. Thyroid hormones seem to have a regulatory role with regard to life span. Hyperthyroid animals appear to have a shorter life and, at advanced age, show a myelin deficit. This may be due to the damage produced by the oxidative stress generated by an excess of thyroid hormones.

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Section: Astrocytes and Neuronesmentioning

confidence: 90%

Thyroid Hormones and the Central Nervous System

Pasquini

Adamo²

1994

Dev Neurosci

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“…Furthermore, antioxidants are low in nerve, and depleted by ROS, leaving the nerves at risk for ROS damage ( Muijsers et al, 1997 ; Romero, 1996 ) . ROS target ion channels, transporters and enzymes ( Konat et al, 1986 ; Kourie, 1998 ; Mattson, 1998 ) , and subtoxic levels facilitate nerve excitability ( Stahl et al, 1993 ) . Increases in ROS have also been implicated in exaggerated pain induced by peripheral nerve injuries ( Khalil et al, 1999 ; Levy et al, 1999 ; Tal, 1996 ; Thomas et al, 1996 ; Wagner et al, 1998 ) (Table 1).…”

Section: Discussionmentioning

confidence: 99%

Sciatic inflammatory neuritis (SIN): Behavioral allodynia is paralleled by peri‐sciatic proinflammatory cytokine and superoxide production

Gazda

Milligan

Hansen

et al. 2001

J Peripheral Nervous Sys

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We have recently developed a model of sciatic inflammatory neuritis (SIN) to assess how immune activation near peripheral nerves influences somatosensory processing. Administration of zymosan (yeast cell walls) around a single sciatic nerve produces dose-dependent low-threshold mechanical allodynia without thermal hyperalgesia. Low (4 microg) doses produce both territorial and extraterritorial allodynia restricted to the injected hindleg. In contrast, higher (40 microg) doses produce territorial and extraterritorial allodynias of both hindlegs, an effect not accounted for by systemic spread of the zymosan. The aim of these experiments was to determine whether these behavioral allodynias were correlated with immunological and/or anatomical changes in or around the sciatic nerve. These experiments reveal that zymosan-induced bilateral allodynia was associated with the following: (a) increased release of both interleukin-1beta and tumor necrosis factor-alpha from peri-sciatic immune cells; (b) increased release of reactive oxygen species from perisciatic immune cells; (c) no change in circulating levels of proinflammatory cytokine; (d) no apparent zymosan-induced influx of immune cells into the sciatic nerve from the endoneurial blood vessels; (e) mild edema of the sciatic, which was predominantly restricted to superficial regions closest to the peri-sciatic immune cells; and (f) no anatomic evidence of changes in either the ipsilateral saphenous nerve or contralateral sciatic nerve that could account for the appearance of extraterritorial or contralateral ("mirror") allodynia, respectively. No reliable differences were found when the low-dose zymosan was compared with vehicle controls. Taken together, these data suggest that substances released by peri-sciatic immune cells may induce changes in the sciatic nerve, leading to the appearance of bilateral allodynia.

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“…This renders the myelin susceptible to degradation by extracellular proteases liberated by macrophages. Lipid peroxidation and protein nitration are the most destructive result of ROS and NO, as these damage a variety of peripheral nerve structures, including ion channels, ATPases, ion transporters, ion exchangers, glucose transporters, membrane-bound enzymes, and mitochondria (149,154,184). Damaged ion channels and transport systems increase neuronal excitability (154,184,283) and alter a variety of second messenger systems via increases in intracellular calcium (154).…”

Section: Antibody-mediated Nerve Damagementioning

confidence: 99%

Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States

Watkins

Maier

2002

Physiological Reviews

656

433

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Chronic pain can occur after peripheral nerve injury, infection, or inflammation. Under such neuropathic pain conditions, sensory processing in the affected body region becomes grossly abnormal. Despite decades of research, currently available drugs largely fail to control such pain. This review explores the possibility that the reason for this failure lies in the fact that such drugs were designed to target neurons rather than immune or glial cells. It describes how immune cells are a natural and inextricable part of skin, peripheral nerves, dorsal root ganglia, and spinal cord. It then examines how immune and glial activation may participate in the etiology and symptomatology of diverse pathological pain states in both humans and laboratory animals. Of the variety of substances released by activated immune and glial cells, proinflammatory cytokines (tumor necrosis factor, interleukin-1, interleukin-6) appear to be of special importance in the creation of peripheral nerve and neuronal hyperexcitability. Although this review focuses on immune modulation of pain, the implications are pervasive. Indeed, all nerves and neurons regardless of modality or function are likely affected by immune and glial activation in the ways described for pain.

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Peroxidative aggregation of myelin membrane proteins

Cited by 12 publications

References 23 publications

Thyroid Hormones and the Central Nervous System

Thyroid Hormones and the Central Nervous System

Sciatic inflammatory neuritis (SIN): Behavioral allodynia is paralleled by peri‐sciatic proinflammatory cytokine and superoxide production

Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States

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