Strain differences in cuprizone induced demyelination

Abstract Background Multiple sclerosis (MS) is a severe neurological disorder, characterized by demyelination of the central nervous system (CNS), and with a prevalence of greater than 2 million people worldwide. In terms of research in MS pathology, the cuprizone toxicity model is widely used. Here...

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Main Authors: Qili Yu, Ryan Hui, Jiyoung Park, Yangyang Huang, Alexander W. Kusnecov, Cheryl F. Dreyfus, Renping Zhou
Format: Article
Language:English
Published: BMC 2017-11-01
Series:Cell & Bioscience
Online Access:http://link.springer.com/article/10.1186/s13578-017-0181-3
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spelling doaj-81ebbae3e9f446b899be37230a7431e02020-11-25T00:31:03ZengBMCCell & Bioscience2045-37012017-11-017111110.1186/s13578-017-0181-3Strain differences in cuprizone induced demyelinationQili Yu0Ryan Hui1Jiyoung Park2Yangyang Huang3Alexander W. Kusnecov4Cheryl F. Dreyfus5Renping Zhou6Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers UniversityDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers UniversityDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers UniversityDepartment of Neuroscience and Cell Biology, Rutgers Robert Wood Johnson Medical SchoolDepartment of Psychology, School of Arts and Sciences, Rutgers UniversityDepartment of Neuroscience and Cell Biology, Rutgers Robert Wood Johnson Medical SchoolDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers UniversityAbstract Background Multiple sclerosis (MS) is a severe neurological disorder, characterized by demyelination of the central nervous system (CNS), and with a prevalence of greater than 2 million people worldwide. In terms of research in MS pathology, the cuprizone toxicity model is widely used. Here we investigated the contribution of genetic differences in response to cuprizone-induced demyelination in two genetically different mouse strains: CD1 and C57BL/6. Results We demonstrate that exposure to a diet containing 0.2% cuprizone resulted in less severe demyelination in the midline of the corpus callosum over the fornix in CD1 mice than C57BL/6 mice. With continuous cuprizone feeding, demyelination in CD1 mice was not prominent until after 7 weeks, in contrast to C57BL/6 mice, which showed prominent demyelination after 4 weeks of exposure. Concomitantly, immunohistochemical analysis demonstrated more oligodendrocytes, as well as fewer oligodendrocyte progenitor cells, microglia and astrocytes in cuprizone treated CD1 mice. We also analyzed 4-weeks-cuprizone treated corpus callosum tissue samples and found that cuprizone treated CD1 mice showed a smaller reduction of myelin-associated glycoprotein (MAG) and a smaller increase of Iba1 and NG2. Conclusions These observations suggest that CD1 mice are less vulnerable to cuprizone-induced demyelination than C57BL/6 mice and thus genetic background factors appear to influence the susceptibility to cuprizone-induced demyelination.http://link.springer.com/article/10.1186/s13578-017-0181-3
collection DOAJ
language English
format Article
sources DOAJ
author Qili Yu
Ryan Hui
Jiyoung Park
Yangyang Huang
Alexander W. Kusnecov
Cheryl F. Dreyfus
Renping Zhou
spellingShingle Qili Yu
Ryan Hui
Jiyoung Park
Yangyang Huang
Alexander W. Kusnecov
Cheryl F. Dreyfus
Renping Zhou
Strain differences in cuprizone induced demyelination
Cell & Bioscience
author_facet Qili Yu
Ryan Hui
Jiyoung Park
Yangyang Huang
Alexander W. Kusnecov
Cheryl F. Dreyfus
Renping Zhou
author_sort Qili Yu
title Strain differences in cuprizone induced demyelination
title_short Strain differences in cuprizone induced demyelination
title_full Strain differences in cuprizone induced demyelination
title_fullStr Strain differences in cuprizone induced demyelination
title_full_unstemmed Strain differences in cuprizone induced demyelination
title_sort strain differences in cuprizone induced demyelination
publisher BMC
series Cell & Bioscience
issn 2045-3701
publishDate 2017-11-01
description Abstract Background Multiple sclerosis (MS) is a severe neurological disorder, characterized by demyelination of the central nervous system (CNS), and with a prevalence of greater than 2 million people worldwide. In terms of research in MS pathology, the cuprizone toxicity model is widely used. Here we investigated the contribution of genetic differences in response to cuprizone-induced demyelination in two genetically different mouse strains: CD1 and C57BL/6. Results We demonstrate that exposure to a diet containing 0.2% cuprizone resulted in less severe demyelination in the midline of the corpus callosum over the fornix in CD1 mice than C57BL/6 mice. With continuous cuprizone feeding, demyelination in CD1 mice was not prominent until after 7 weeks, in contrast to C57BL/6 mice, which showed prominent demyelination after 4 weeks of exposure. Concomitantly, immunohistochemical analysis demonstrated more oligodendrocytes, as well as fewer oligodendrocyte progenitor cells, microglia and astrocytes in cuprizone treated CD1 mice. We also analyzed 4-weeks-cuprizone treated corpus callosum tissue samples and found that cuprizone treated CD1 mice showed a smaller reduction of myelin-associated glycoprotein (MAG) and a smaller increase of Iba1 and NG2. Conclusions These observations suggest that CD1 mice are less vulnerable to cuprizone-induced demyelination than C57BL/6 mice and thus genetic background factors appear to influence the susceptibility to cuprizone-induced demyelination.
url http://link.springer.com/article/10.1186/s13578-017-0181-3
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AT alexanderwkusnecov straindifferencesincuprizoneinduceddemyelination
AT cherylfdreyfus straindifferencesincuprizoneinduceddemyelination
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