Normal Cerebellar Development in S100B-Deficient Mice
Normal Cerebellar Development in S100B-Deficient Mice
复制标题
DOI：
10.1007/s12311-014-0606-z
复制
发表时间：
2015-04-01
期刊：
影响因子：
3.5
通讯作者：
Lohr, Christian
中科院分区：
文献类型：
--
作者：
Bluhm, Bjoern;Laffer, Bjoern;Lohr, Christian
钙结合蛋白S100 B已被证明在体外支持神经元增殖、迁移和轴突生长，而S100 B在体内对神经元发育的意义是有争议的。我们研究了S100B缺陷对出生后5天和10天（P5和P10）S100B基因敲除小鼠小脑发育的影响。这个时间范围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状生长。Bergmann胶质细胞含有特别高浓度的S100 B，并作为迁移颗粒细胞和生长浦肯野细胞树突的支架。这使得出生后小脑理想的模型系统，以研究S100 B的神经胶质细胞和神经元发育的重要性。我们测量了Bergmann胶质细胞突起的长度，外部颗粒细胞层的宽度作为颗粒细胞增殖的量度，外部颗粒细胞层的宽度在P5和P10之间的减少作为颗粒细胞迁移的量度，以及野生型和S100B基因敲除小鼠中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表现相同。结果表明，S100B缺陷小鼠小脑发育正常，运动功能无严重损害。
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.