Estudo ultra-estrutural do processo remielinizante pós-injeção de brometo de etídio no tronco encefálico de ratos imunossuprimidos com dexametasona

Bondan, Eduardo F.; Lallo, Maria Anete; Baz, Erika Infante; Sinhorini, I L; Graça, Dominguita Lühers

doi:10.1590/s0004-282x2004000100023

Cited by 10 publications

(16 citation statements)

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“…The finding of huge amounts of myelin-derived membranes in the PNS demyelinating lesions of diabetic rats resembled the one observed in the brainstem of rats immunosuppressed with cyclophosphamide 3 or dexamethasone 4 as well as in streptozotocin-diabetic rats 5 in which was observed a delay in the scavenging activi-ty of macrophages and in the subsequent CNS remyelinating process. Short-term diabetes mimics lesions of slow development induced by EB in the rat CNS and delays all the subsequent repair events 5 .…”

Section: Discussionsupporting

confidence: 71%

“…Several studies reported the invasive capacity of Schwann cells into the CNS from spinal or cranial nerves due to the glia limitans disruption following injection of the gliotoxin [1][2][3][4][5] . This invasion however appeared to be diminished in the diabetic state induced by streptozotocin treatment 6 .…”

Section: Discussionmentioning

confidence: 99%

“…The gliotoxic agent ethidium bromide (EB) induces early astrocyte disappearance and oligodendroglial loss when injected in the central nervous system (CNS) leading to blood-brain barrier disruption and primary demyelination respectively. Subsequent remyelination occurs performed by surviving oligodendrocytes and by invasive Schwann cells [1][2][3][4][5][6] . After local EB injection in the peripheral nervous system (PNS) no destruction of myelinating cells but rather intoxication of Schwann cells is observed 7 .…”

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Ethidium bromide-induced demyelination in the sciatic nerve of diabetic rats

Bondan

Custódio

Lallo

et al. 2009

Arq. Neuro-Psiquiatr.

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-This study aims to observe the process of myelin loss and repair following the injection of the gliotoxic agent ethidium bromide (EB) in the sciatic nerve of rats previously induced to diabetes mellitus by streptozotocin. Injection of EB was also done in non-diabetic rats. The animals were euthanatized from 3 to 31 days after intraneural injection and nerve sections were collected for ultrastructural study. In nondiabetic rats, Schwann cells (CS) showed signs of intoxication 3 days after, with cytoplasmic vacuolization and rejection of their myelin sheaths. Myelin debris were removed by macrophages in the endoneurium and mast cells were abundant in the lesions. From 14 days following EB injection, supernumerary CS were seen in the expanded endoneurium as well as thin myelin sheaths indicating remyelination. Diabetic rats presented a more extensive myelin vesiculation and segmentar demyelination, with delayed activities from both macrophages and remyelinating SC. No mast cells were noted.KEY WORDS: demyelination, diabetes mellitus, ethidium bromide, peripheral nervous system, remyelination, Schwann cells.desmielinização induzida pelo brometo de etídio no nervo ciático de ratos diabéticos resumo -O estudo visa à observação do processo de perda e reparo mielínico pós-injeção do gliotóxico brometo de etídio (BE) no nervo ciático de ratos previamente induzidos a diabetes mellitus pela estreptozotocina. Injeção de BE foi igualmente realizada em ratos não-diabéticos. Os animais foram eutanasiados dos 3 aos 31 dias pós-injeção intraneural, com colheita de amostras neurais para estudo ultraestrutural. Nos animais não-diabéticos, as células de Schwann (CS) mostraram sinais de intoxicação a partir dos 3 dias pós-gliotóxico, com vacuolização citoplasmática e rejeição de suas bainhas de mielina. Restos mielínicos eram removidos por macrófagos no interior do endoneuro e mastócitos eram abundantes nas lesões. A partir dos 14 dias, CS supranumerárias foram encontradas no endoneuro expandido, além de finas bainhas de mielina indicativas de remielinização. Os ratos diabéticos apresentaram vesiculação mielínica e desmielinização segmentar mais extensas, bem como ausência de mastócitos e atraso na atividade macrofágica e na função remielinizante das CS. PALAVRAS-CHAVE: brometo de estídio, células de Schwann, desmielinização, diabetes mellitus, remielinização, sistema nervoso periférico.

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Section: Discussionsupporting

confidence: 71%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Ethidium bromide-induced demyelination in the sciatic nerve of diabetic rats

Bondan

Custódio

Lallo

et al. 2009

Arq. Neuro-Psiquiatr.

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“…It is characterized as an auto-immune disease that causes destruction of oligodendrocytes and, consequently, loss of the myelin sheath. This myelin loss causes a great variability of pathologic conditions [2][3][4] . Although its etiology is unknown 5 , it is postulated that genetic and environmental factors causes self-destructive lesions in the central nervous system, specifically against the white matter [5][6][7] .…”

Section: Ft Cíntia Cristina Souza Nassar -Rua Voluntários Da Pátria mentioning

confidence: 99%

“…Numerous experimental models that simulate the pathophysiology of the demyelinating process of Ms have been developed. ethidium bromide (eB) is a gliotoxic drug that induces demyelination 2,3 and it is a well described model that has improved the comprehension of the biologic process of central nervous system (cNs) demyelination [11][12][13] .…”

Section: Ft Cíntia Cristina Souza Nassar -Rua Voluntários Da Pátria mentioning

confidence: 99%

Effects of aquatic exercises in a rat model of brainstem demyelination with ethidium bromide on the beam walking test

Nassar

Bondan

Alouche

2009

Arq. Neuro-Psiquiatr.

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-Multiple sclerosis is a demyelinating disease of the central nervous system associated with varied levels of disability. The impact of early physiotherapeutic interventions in the disease progression is unknown. We used an experimental model of demyelination with the gliotoxic agent ethidium bromide and early aquatic exercises to evaluate the motor performance of the animals. We quantified the number of footsteps and errors during the beam walking test. The demyelinated animals walked fewer steps with a greater number of errors than the control group. The demyelinated animals that performed aquatic exercises presented a better motor performance than those that did not exercise. Therefore aquatic exercising was beneficial to the motor performance of rats in this experimental model of demyelination.Key Words: multiple sclerosis, demyelination, aquatic exercises, physiotherapy.Efeitos de exercícios aquáticos no desempenho motor de ratos submetidos a um modelo de desmielização com brometo de etídio resumo -A esclerose múltipla é uma doença desmielinizante do sistema nervoso central que se associa a graus variados de incapacidade. Não se sabe se a realização de intervenções fisioterapêuticas precoces têm impacto na evolução dessa doença. Utilizamos um modelo experimental de desmielinização com o gliotóxico brometo de etídio e a aplicação de exercícios aquáticos precoces para avaliar o desempenho motor dos animais. Foram quantificados o número de passos e os erros executados durante a travessia da barra elevada. os animais desmielinizados apresentaram menor número de passos e maior quantidade de erros em comparação aos grupos-controle. os animais desmielinizados que realizaram exercícios aquáticos apresentaram melhor desempenho motor que os animais desmielinizados que não foram submetidos à intervenção. Portanto, a realização de exercícios aquáticos mostrou-se benéfica no desempenho motor dos animais submetidos ao modelo experimental do brometo de etídio.PAlAvrAs-chAve: esclerose múltipla, desmielinização, exercícios aquáticos, fisioterapia.

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