通过FLRT粘附分子控制神经元迁移来调节大脑皮层折叠
Daniel Del Toro1, Tobias Ruff1, Erik Cederfjäll1
1Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152 Martinsried, Germany.
Cell
|May 6, 2017
概括
神经元粘附分子FLRT1和FLRT3的变化通过改变神经元迁移而不是祖细胞放大来驱动哺乳动物大脑皮层的折叠. 这表明细胞间粘附是物种间皮层折叠的关键.
科学领域:
- 神经科学
- 发育生物学
- 遗传学
背景情况:
- 在哺乳动物大脑功能中,
- 这一过程传统上与祖细胞放大和接触性迁移有关.
研究的目的:
- 阐明皮层折叠背后的分子机制.
- 研究神经元迁移和细胞间粘附在这个过程中的作用.
主要方法:
- 使用了FLRT1和FLRT3粘附分子缺失的小鼠模型.
- 分析皮层结构,原生细胞群和神经元迁移模式.
- 进行计算分析和模拟.
主要成果:
- FLRT1/3的删除导致了完整的层次组织的宏观皮质折叠 (sulci).
- 皮层折叠取决于神经元迁移的改变,而不是祖细胞放大.
- 细胞间粘附的减少和神经元迁移的增加导致皮质板块的聚合,促进硫的形成.
- 在人类和驼皮层中观察到低FLRT1 / 3表达,特别是在发育的皮区域.
结论:
- 由FLRT1/3调节的细胞间粘附是皮层折叠的关键决定因素.
- 神经元迁移动力学受到粘附的影响,在塑造大脑皮层方面发挥着重要作用.
- 这些发现突显了哺乳动物物种中皮层折叠的保存机制.
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