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S100B基因缺陷小鼠的小脑正常发育

Normal cerebellar development in S100B-deficient mice.

作者信息

Bluhm Björn, Laffer Björn, Hirnet Daniela, Rothermundt Matthias, Ambree Oliver, Lohr Christian

机构信息

Division of Neurophysiology, Biocenter Grindel, Martin-Luther-King-Pl. 3, D-20146, Hamburg, Germany.

出版信息

Cerebellum. 2015 Apr;14(2):119-27. doi: 10.1007/s12311-014-0606-z.

DOI:10.1007/s12311-014-0606-z
PMID:25342137
Abstract

The calcium-binding protein S100B has been shown to support neuron proliferation, migration and neurite growth in vitro, while the significance of S100B for neuronal development in vivo is controversial. We have investigated the effect of S100B deficiency on cerebellar development in S100B knockout mice at an age of 5 and 10 days after birth (P5 and P10). This time range covers important developmental steps in the cerebellum such as granule cell proliferation and migration, as well as dendritic growth of Purkinje cells. Bergmann glial cells contain a particularly high concentration of S100B and serve as scaffold for both migrating granule cells and growing Purkinje cell dendrites. This renders the postnatal cerebellum ideal as a model system to study the importance of S100B for glial and neuronal development. We measured the length of Bergmann glial processes, the width of the external granule cell layer as a measure of granule cell proliferation, the decrease in width of the external granule cell layer between P5 and P10 as a measure of granule cell migration, and the length of Purkinje cell dendrites in wild-type and S100B knockout mice. None of these parameters showed significant differences between wild-type and knockout mice. In addition, wild-type and knockout mice performed equally in locomotor behaviour tests. The results indicate that S100B-deficient mice have normal development of the cerebellum and no severe impairment of motor function.

摘要

钙结合蛋白S100B已被证明在体外可支持神经元增殖、迁移和神经突生长,而S100B在体内神经元发育中的意义仍存在争议。我们研究了S100B基因敲除小鼠出生后5天和10天(P5和P10)时S100B缺乏对小脑发育的影响。这个时间段涵盖了小脑中重要的发育步骤,如颗粒细胞增殖和迁移,以及浦肯野细胞的树突生长。伯格曼胶质细胞含有特别高浓度的S100B,并为迁移的颗粒细胞和生长的浦肯野细胞树突提供支架。这使得出生后的小脑成为研究S100B对胶质细胞和神经元发育重要性的理想模型系统。我们测量了野生型和S100B基因敲除小鼠中伯格曼胶质细胞突起的长度、作为颗粒细胞增殖指标的外颗粒细胞层宽度、作为颗粒细胞迁移指标的P5和P10之间外颗粒细胞层宽度的减少,以及浦肯野细胞树突的长度。这些参数在野生型和基因敲除小鼠之间均未显示出显著差异。此外,野生型和基因敲除小鼠在运动行为测试中的表现相当。结果表明,S100B缺乏的小鼠小脑发育正常,运动功能无严重受损。

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Serum S100β Levels Are Linked with Cognitive Decline and Peripheral Inflammation in Spinocerebellar Ataxia Type 2.血清 S100β 水平与脊髓小脑性共济失调 2 型的认知下降和外周炎症有关。
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