Kálmán Mihály, Oszwald Erzsébet, Pócsai Károly, Bagyura Zsolt, Adorján István
Department of Anatomy, Histology, Embryology, Semmelweis University, Budapest, Hungary.
Department of Anatomy, Histology, Embryology, Semmelweis University, Budapest, Hungary; Department of Physiology, Anatomy, Genetics, Univ. of Oxford, UK.
Int J Dev Neurosci. 2018 Oct;69:97-105. doi: 10.1016/j.ijdevneu.2018.07.003. Epub 2018 Jul 20.
The present paper provides novel findings on the temporo-spatial correlation of perivascular laminin immunoreactivity with the early postnatal astrocyte development. The cerebrovascular laminin immunoreactivity gradually disappears during development. The fusion of the glial and vascular basal laminae during development makes the laminin epitopes inaccessible for antibody molecules (Krum et al., 1991, Exp Neurol 111:151). The fusion is supposed to correlate with the maturation of the glio-vascular connections. Glial development was followed by immunostaining for GFAP (glial fibrillary acidic protein), S100 protein, glutamine synthetase as glial markers and for nestin to visualize the immature glial structures. Our investigation focused on the period from postnatal day (P)2 to P16, on the dorso-parietal pallium. In the wall of the telencephalon the laminin immunoreactivity disappeared between P5 and P10; in subcortical structures it persisted to P12 or even to P16. Its disappearance overlapped the period when GFAP-immunopositive astrocytes were taking the place of radial glia. Despite the parallel time courses, however, the spatial patterns of the two processes were just the opposite: disappearance of the laminin immunoreactivity progressed from the middle zone whereas the appearance of GFAP from the pial surface and the corpus callosum. Rather, the regression of the vascular laminin immunoreactivity followed the progression of the immunoreactivities of glutamine synthetase and S100 protein. Therefore, the regression really correlates with a 'maturation' of astrocytes which, however, affects other astrocyte functions rather than cytoskeleton.
本文提供了关于血管周围层粘连蛋白免疫反应性与出生后早期星形胶质细胞发育的时空相关性的新发现。脑血管层粘连蛋白免疫反应性在发育过程中逐渐消失。发育过程中神经胶质和血管基底膜的融合使层粘连蛋白表位无法被抗体分子识别（Krum等人，1991年，《实验神经病学》111:151）。这种融合被认为与神经胶质-血管连接的成熟有关。通过对胶质纤维酸性蛋白（GFAP）、S100蛋白、谷氨酰胺合成酶进行免疫染色作为神经胶质标记物，并对巢蛋白进行免疫染色以观察未成熟的神经胶质结构，来跟踪神经胶质的发育。我们的研究集中在出生后第（P）2天至P16天的背顶叶皮质。在端脑壁中，层粘连蛋白免疫反应性在P5和P10之间消失；在皮质下结构中，它持续到P12甚至P16。其消失与GFAP免疫阳性星形胶质细胞取代放射状胶质细胞的时期重叠。然而，尽管这两个过程的时间进程平行，但它们的空间模式却相反：层粘连蛋白免疫反应性的消失从中部区域开始，而GFAP的出现则从软脑膜表面和胼胝体开始。相反，血管层粘连蛋白免疫反应性的消退跟随谷氨酰胺合成酶和S100蛋白免疫反应性的进展。因此，这种消退实际上与星形胶质细胞的“成熟”相关，然而，这影响的是其他星形胶质细胞功能而非细胞骨架。
