AI Article Synopsis
- * This research examined changes at the axon-myelin interface using advanced microscopy techniques and showed that cuprizone exposure leads to non-inflammatory damage in oligodendrocytes, causing vacuole formation in myelin and swelling of axons.
- * The similarities found in the ultrastructural features of myelin between multiple sclerosis and the cuprizone model suggest that the cuprizone model is useful for studying the initial stages of lesion formation.
Article Abstract
Myelin damage is a histopathological hallmark of multiple sclerosis lesions. Results of studies suggest that impaired myelin-axon interaction characterized by focal myelin detachments is an early event during lesion genesis. In this study, we investigated the ultrastructural changes of the axon-myelin interface in the cuprizone model using serial block face scanning electron microscopy and immunohistochemistry. We show that non-inflammatory injury of oligodendrocytes by cuprizone intoxication results in myelin vacuole formation and axonal swellings, paralleled by early alterations of the node of Ranvier cytoarchitecture. This remarkable resemblance of ultrastructural myelin characteristics in multiple sclerosis and the cuprizone animal model suggests that the cuprizone model is a valuable tool to study early pathologies during lesion formation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8895267 | PMC |
| http://dx.doi.org/10.3389/fncel.2022.709596 | DOI Listing |
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Article Synopsis
- This study investigates how chronic demyelination affects the hypothalamic-pituitary-gonadal axis in a mouse model of multiple sclerosis.
- Adult male mice were divided into a control group and an experimental group fed with cuprizone (CPZ), revealing significant decreases in myelin content, testosterone levels, and reproductive parameters in the CPZ group.
- The findings suggest that long-term CPZ-induced demyelination may disrupt the hormone axis and impair testicular function and sperm production, likely due to hypothalamic damage.
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