Kiss J Z, Wang C, Rougon G
Institute of Histology and Embryology, University of Geneva Medical School, Switzerland.
Neuroscience. 1993 Mar;53(1):213-21. doi: 10.1016/0306-4522(93)90299-u.
The adult hypothalamo-neurohypophysial system of the rat retains the capacity to express highly polysialylated isoforms of neural cell adhesion molecule normally expressed in developing tissues. Here we report that the expression of these isoforms in neurohypophysial astrocytes (pituicytes) may be regulated by neurosecretory cells. In the intact neurohypophysis a strong and homogeneously distributed immunostaining for the "embryonic", highly sialylated form of neural cell adhesion molecules was detected by light-microscopic immunocytochemistry. By electron-microscopy, both neurosecretory axons and pituicytes were immunoreactive for this isoform. However, in contrast to the rather uniform staining on nerve fibres, polysialic acid immunolabelling on glial surfaces was uneven: immunostaining could be observed on glial surfaces facing neuronal elements, but not at contact sites between pituicytes. In addition, most glial and neuronal elements were heavily and evenly labelled with the polyclonal antibody recognizing "total" neural cell adhesion molecule. Surgical transection of the hypophysial stalk, a procedure that eliminates descending neurosecretory axons from the neurohypophysis, resulted in the complete disappearance of polysialic immunoreactivity from the neurohypophysis. The electron-microscopic analysis confirmed that cell surfaces of pituicytes lacked this immunoreactivity after the lesion. When residual neurosecretory axons were observed following an incomplete lesion, immunoreactivity on axons and glial processes was maintained. Transection did not affect the distribution of "total" neural cell adhesion molecule. We postulate that the presence of neurosecretory axons in the neurohypophysis is necessary to maintain the capacity of pituicytes to express immunoreactivity for the polysialylated isoforms of neural cell adhesion molecule but not the neural cell adhesion molecule itself since immunoreactivity for "total" neural cell adhesion molecule was unaltered after hypophysial stalk transection.(ABSTRACT TRUNCATED AT 250 WORDS)
大鼠的成年下丘脑 - 神经垂体系统保留了表达在发育组织中正常表达的高度多唾液酸化神经细胞粘附分子亚型的能力。在此我们报告，这些亚型在神经垂体星形胶质细胞（垂体细胞）中的表达可能受神经分泌细胞调控。在完整的神经垂体中，通过光学显微镜免疫细胞化学检测到针对神经细胞粘附分子的“胚胎型”、高度唾液酸化形式的强且均匀分布的免疫染色。通过电子显微镜观察，神经分泌轴突和垂体细胞对该亚型均有免疫反应性。然而，与神经纤维上相当均匀的染色不同，胶质细胞表面的多唾液酸免疫标记并不均匀：在面向神经元成分的胶质细胞表面可观察到免疫染色，但在垂体细胞之间的接触部位则没有。此外，大多数胶质细胞和神经元成分都被识别“总”神经细胞粘附分子的多克隆抗体大量且均匀地标记。垂体柄的手术横断，这一消除从神经垂体下行的神经分泌轴突的操作，导致神经垂体中多唾液酸免疫反应性完全消失。电子显微镜分析证实，损伤后垂体细胞的细胞表面缺乏这种免疫反应性。当不完全损伤后观察到残留的神经分泌轴突时，轴突和胶质细胞突起上的免疫反应性得以维持。横断并未影响“总”神经细胞粘附分子的分布。我们推测，神经垂体中神经分泌轴突的存在对于维持垂体细胞表达神经细胞粘附分子多唾液酸化亚型免疫反应性的能力是必要的，但对于神经细胞粘附分子本身并非如此，因为垂体柄横断后“总”神经细胞粘附分子的免疫反应性未改变。（摘要截选至250词）
