Early microglial colonization of the human forebrain and possible involvement in periventricular white‐matter injury of preterm infants

Early microglial colonization of the human forebrain and possible involvement in periventricular white‐matter injury of preterm infants
复制标题

DOI:
10.1111/j.1469-7580.2010.01245.x
复制
发表时间:
2010-10
期刊:
影响因子:
2.4
通讯作者:
C. Verney;A. Monier;C. Fallet-Bianco;P. Gressens
C. Verney;A. Monier;C. Fallet-Bianco;P. Gressens
中科院分区:
医学3区
文献类型:
--
作者:
C. Verney;A. Monier;C. Fallet-Bianco;P. Gressens

文献摘要

被引文献

相似文献

通过针对离子钙结合衔接分子1、CD 68和CD 45的抗体可视化的变形样小胶质细胞亚群在排卵后或妊娠后4.5周(gw)开始进入前脑。它们通过脑膜、脉络丛和脑室区穿透端脑和间脑。变形小胶质细胞-巨噬细胞的早期定殖首先限于白色物质,这些细胞在其中迁移并在白色物质通路的连接处以斑块形式聚集,例如内囊分别与丘脑皮质投射、外囊和大脑脚形成的三个连接处。在大脑皮质原基中,迁移主要是径向和切向未成熟的白色物质、基板层和皮质板,而软脑膜细胞则分布在预期的第I层。第二波小胶质细胞以约12-13 gw通过血管途径穿透大脑,并保持局限于白色物质。有两个主要的调查结果值得强调。首先,小胶质细胞在皮质板-亚板连接处积累10-12 gw,在那里检测到第一个突触。第二,小胶质细胞聚集在限制性层状带中,最明显的是在白色物质(半卵圆中心)的轴突交叉点处的19-30 gw左右,在未成熟的白色物质中向尾侧延伸到视觉辐射。这种增殖小胶质细胞的积聚位于早产儿的白色物质损伤部位。小胶质细胞在未成熟的白色和灰质中的时空组织表明,这些细胞可能在发育过程中发挥积极作用,如轴突导向、突触发生和神经发育凋亡,以及发育中大脑的损伤,特别是早产儿的脑室周围白色-物质损伤。
Amoeboid microglial subpopulations visualized by antibodies against ionized calcium‐binding adapter molecule 1, CD68, and CD45 enter the forebrain starting at 4.5 postovulatory or gestational weeks (gw). They penetrate the telencephalon and diencephalon via the meninges, choroid plexus, and ventricular zone. Early colonization by amoeboid microglia–macrophages is first restricted to the white matter, where these cells migrate and accumulate in patches at the junctions of white‐matter pathways, such as the three junctions that the internal capsule makes with the thalamocortical projection, external capsule and cerebral peduncle, respectively. In the cerebral cortex anlage, migration is mainly radial and tangential towards the immature white matter, subplate layer, and cortical plate, whereas pial cells populate the prospective layer I. A second wave of microglial cells penetrates the brain via the vascular route at about 12–13 gw and remains confined to the white matter. Two main findings deserve emphasis. First, microglia accumulate at 10–12 gw at the cortical plate–subplate junction, where the first synapses are detected. Second, microglia accumulate in restricted laminar bands, most notably around 19–30 gw, at the axonal crossroads in the white matter (semiovale centre) rostrally, extending caudally in the immature white matter to the visual radiations. This accumulation of proliferating microglia is located at the site of white‐matter injury in premature neonates. The spatiotemporal organization of microglia in the immature white and grey matter suggests that these cells may play active roles in developmental processes such as axonal guidance, synaptogenesis, and neurodevelopmental apoptosis as well as in injuries to the developing brain, in particular in the periventricular white‐matter injury of preterm infants.