The hippocampal fimbria of cuprizone-treated animals as a structure for studying neuroprotection in multiple sclerosis.

The hippocampal fimbria of cuprizone-treated animals as a structure for studying neuroprotection in multiple sclerosis.
复制标题

DOI:
10.1007/s00011-011-0339-0
复制
发表时间:
2011-08
影响因子:
6.7
通讯作者:
Beyer, C.
Beyer, C.
中科院分区:
医学2区
文献类型:
--
作者:
Kipp, M.;Norkus, A.;Krauspe, B.;Clarner, T.;Berger, K.;van der Valk, P.;Amor, S.;Beyer, C.

文献摘要

参考文献

被引文献

相似文献

已经证明多发性硬化症中外观正常的白色物质(NAWM)的变化先于经典病变的出现。在已建立的疾病模型中对NAWM生物学的理解可能有助于阐明为什么其中一些进展为活动性脱髓鞘病变。本研究中使用C57 BL 6雄性小鼠(19-21 g)。通过给小鼠喂食含有0.2%铜宗的饮食长达5周来诱导脱髓鞘。进行常规染色(luxol坚牢蓝、苏木精和伊红)和免疫组织化学以评估髓鞘状态和炎性浸润。我们证明,在毒性脱髓鞘铜环模型中,胼胝体在5周铜环攻击后严重脱髓鞘(急性脱髓鞘),而海马伞在常规髓鞘染色中显示正常。急性脱髓鞘后海马伞明显可见小胶质细胞增生,但星形胶质细胞增生不明显。有趣的是,这两个区域,海马伞和胼胝体,表现出早期少突胶质细胞凋亡以及强烈的小胶质细胞积累和激活。然而,只有胼胝体进展为活跃的脱髓鞘病变,而海马伞则不会。所应用的模型似乎适合于阐明促进受影响组织进展为活动性病变的途径。
It has been demonstrated that changes in the normal-appearing white matter (NAWM) in multiple sclerosis precede the appearance of classical lesions. The understanding of NAWM biology in an established disease model might help to clarify why some of them progress to active demyelinating lesions. C57BL6 male mice (19–21 g) were used in this study. Demyelination was induced by feeding mice a diet containing 0.2% cuprizone for up to 5 weeks. Routine stainings (luxol fast blue, and hematoxylin and eosin) and immunohistochemistry were performed to assess myelin status and the inflammatory infiltrate. We demonstrated that, in the toxic demyelination cuprizone model, the corpus callosum is severely demyelinated after a 5-week cuprizone challenge (acute demyelination) whereas the fimbria of the hippocampus appear normal in routine myelin stainings. Microgliosis but not astrogliosis is evident after acute demyelination in the fimbria. Interestingly, both regions, the fimbria and the corpus callosum, demonstrated early oligodendrocyte apoptosis as well as intense microglia accumulation and activation. However, only the corpus callosum progresses to actively demyelination lesions whereas the fimbria does not. The applied model appears suitable for elucidating pathways which promote progression of affected tissue to an active lesion.
DOI: 10.1002/glia.20663
发表时间: 2008-06-01
期刊: GLIA
影响因子: 6.2
作者:
De Haas, Alexander H.;Boddeke, Hendrikus W. G. M.;Biber, Knut
通讯作者: Biber, Knut
DOI: 10.1212/wnl.45.3.478
发表时间: 1995-03-01
期刊: NEUROLOGY
影响因子: 9.9
作者:
FILIPPI, M;CAMPI, A;COMI, G
通讯作者: COMI, G
DOI: 10.1093/brain/121.1.103
发表时间: 1998-01-01
期刊: BRAIN
影响因子: 14.5
作者:
Fu, L;Matthews, PM;Arnold, DL
通讯作者: Arnold, DL
DOI: 10.1093/brain/awm291
发表时间: 2008-01-01
期刊: BRAIN
影响因子: 14.5
作者:
Zeis, Thomas;Graumann, Ursula;Schaeren-Wiemers, Nicole
通讯作者: Schaeren-Wiemers, Nicole
DOI: 10.1016/0022-510x(79)90142-4
发表时间: 1979-01-01
影响因子: 4.4
作者:
ALLEN, IV;MCKEOWN, SR
通讯作者: MCKEOWN, SR