A technique for producing demyelination of the rat optic nerves

Guazzo, E.

doi:10.1016/j.jocn.2004.08.002

Cited by 25 publications

(17 citation statements)

References 7 publications

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“…MS affects optic apparatus particularly optic chiasm and nerves in more than 70% of the patients (Otradovec 1965;Beck et al 1983;Guazzo 2005). Our data demonstrated that structural and molecular changes, during demyelination and remyelination processes of adult optic chiasm and nerves, correlate with each other and with those of our previously described electrophysiologic results.…”

Section: Discussionsupporting

confidence: 83%

Analysis of Structural and Molecular Events Associated with Adult Rat Optic Chiasm and Nerves Demyelination and Remyelination; Possible Role for 3rd Ventricle Proliferating Cells

et al. 2011

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Multiple sclerosis frequently affects the optic apparatus, particularly optic chiasm and nerves. Here, we have reported the structural and molecular characteristics of remyelination in the adult rat optic chiasm and nerves. Moreover, considering the proximity of optic chiasm and 3rd ventricle, we have tried to determine if proliferating cells residing in 3rd ventricle region are able to migrate in response to experimental demyelination of the optic chiasm. Following local demyelination by lysolecithin, remyelination pattern in longitude of optic chiasm and proximal nerves was investigated using myelin staining and marker genes expression. Furthermore, cell tracing was carried out using BrdU labeling of proliferating cells prior to gliotoxin injection. Morphometric analysis revealed that demyelination was considerable on days 7 and 14 and an incomplete remyelination occurred on day 28 post-lesion. Interestingly, myelin repair was more evident in the caudal part of chiasm, compared to rostral part and proximal optic nerves. Following chiasm and nerve demyelination, trains of BrdU+ cells were seen near the 3rd ventricle which subsequently moved to lesion site. Nestin was significantly up-regulated in 3rd ventricle surroundings. At the lesion site, Nogo-A gene expression was significantly decreased on days 7 and 14 post lesion, while Olig2, nestin, and GFAP expression was increased on day 7. The changes were then reversed by the time. Myelin repair in optic chiasm seems to be mediated by endogenous progenitors and stem cells. Adult 3rd ventricle proliferating cells may play a role in this context by mobilization into the demyelinated chiasm.

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Section: Discussionsupporting

confidence: 83%

Analysis of Structural and Molecular Events Associated with Adult Rat Optic Chiasm and Nerves Demyelination and Remyelination; Possible Role for 3rd Ventricle Proliferating Cells

et al. 2011

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“…However, a study that correlates apyrase and 5¢-nucleotidase activities with an experimental model of demyelination was not found in the literature. In the present study, we used the gliotoxic model induced by EB, which has been extensively studied, showing good reproducibility of demyelination, and is considered a commonly used model to explore the reparative capacity of the CNS [21,[25][26][27]40]. This work was carried out in order to investigate possible changes in apyrase and 5¢-nucleotidase activities in synaptosomes at different time periods after the injection of EB in the rat's brainstem.…”

Section: Discussionmentioning

confidence: 99%

“…Many animal models have been utilized for mimicking demyelination and remyelination events of MS [23,24], as for example, the toxic model induced by ethidium bromide (EB). EB is a substance that produces demyelination in the CNS by destroying, mainly, neuroglial cells, astrocytes and oligodendrocytes [25,26].…”

Section: Introductionmentioning

confidence: 99%

Apyrase and 5′-nucleotidase Activities in Synaptosomes from the Cerebral Cortex of Rats Experimentally Demyelinated with Ethidium Bromide and Treated with Interferon-β

et al. 2006

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Apyrase and 5'-nucleotidase activities were analyzed in an ethidium bromide (EB) demyelinating model associated with interferon-beta (IFN-beta). The animals were divided in groups: I, control (saline); II, saline and IFN-beta; III, EB and IV, EB and IFN-beta. After 7, 15 and 30 days the animals (n = 5) were sacrificed and the cerebral cortex was removed for synaptosome preparation and enzymatic assays. Apyrase activity using ATP as substrate increased in groups II, III and IV (P < 0.001) after 7 days and in groups III and IV (P < 0.001) after 15 days. Using ADP as substrate, an activation of this enzyme was observed in group III (P < 0.05) after seven and 15 days. The 5'-nucleotidase activity increased in group III (P < 0.05) after 7 days and in groups II, III and IV (P < 0.001) after 15 days. After 30 days treatment, no significant alteration was observed in enzyme activities. Results showed that apyrase and 5'-nucleotidase activities are altered in demyelination events and that IFN-beta was able to regulate the adenine nucleotide hydrolysis.

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“…Direct injection of ethidium bromide (EB) as a chromatin-disrupting agent has offered a simple, reproducible, and powerful model for studying the biology of remyelination and the subsequent repair process (Blakemore 1982;Woodruff and Franklin 1998). Oligodendroglial damage induced by EB produces cell death and primary demyelinating lesions at the site of injection (Blakemore et al 1983;Bondan et al 2000Bondan et al , 2006Guazzo 2005). Reactive T cells and macrophages in CNS produce cytokines and other mediators like tumor necrosis factor a, interferon c, and reactive oxygen species (H 2 O 2 , O 2 -, NO) that activate caspase protein family (Rus et al 2006).…”

Section: Introductionmentioning

confidence: 99%

Vitamins E and D3 Attenuate Demyelination and Potentiate Remyelination Processes of Hippocampal Formation of Rats Following Local Injection of Ethidium Bromide

et al. 2009

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Cognitive deficits have been observed in patients with multiple sclerosis (MS) due to hippocampal insults. Antioxidant vitamins D and E are suggested for patients suffering from neurodegenerative diseases like MS, while their mechanisms of action are not well understood. Here, we have tried to study the effects of these vitamins on demyelination, cell death, and remyelination of rat hippocampus following local ethidium bromide (EB) injection. Animals received 100 mg/kg vitamin E or 5 microg/kg of vitamin D3 for 2, 7, or 28 days. The extent of demyelination, myelin staining intensity, and expression of myelin basic protein and caspase-3 were investigated using histological and immunoblotting verification. Administration of EB alone caused demyelination, cell death, and afterward an endogenous repair. Vitamins E and D3 reduced the EB-induced damage and increased the endogenous remyelination of hippocampus. Although the anti-apoptotic effect of these vitamins and protection against demyelination were predictable based on their antioxidant effect, our results indicated the positive effect of vitamins E and D3 on process of remyelination by endogenous progenitor cells and supported their possible therapeutic effects in the context of demyelinating diseases like MS.

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A technique for producing demyelination of the rat optic nerves

Cited by 25 publications

References 7 publications

Analysis of Structural and Molecular Events Associated with Adult Rat Optic Chiasm and Nerves Demyelination and Remyelination; Possible Role for 3rd Ventricle Proliferating Cells

Analysis of Structural and Molecular Events Associated with Adult Rat Optic Chiasm and Nerves Demyelination and Remyelination; Possible Role for 3rd Ventricle Proliferating Cells

Apyrase and 5′-nucleotidase Activities in Synaptosomes from the Cerebral Cortex of Rats Experimentally Demyelinated with Ethidium Bromide and Treated with Interferon-β

Vitamins E and D3 Attenuate Demyelination and Potentiate Remyelination Processes of Hippocampal Formation of Rats Following Local Injection of Ethidium Bromide

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