Kaur C, Wu C H, Wen C Y, Ling E A
Department of Anatomy, National University of Singapore.
Arch Histol Cytol. 1994 Dec;57(5):449-59. doi: 10.1679/aohc.57.449.
Subcutaneous injections of glucocorticoids into postnatal rats resulted in a drastic reduction in the number of amoeboid microglial cells in the corpus callosum as shown by their labelling with the monoclonal antibodies of the OX-series, ED1, lectin and rhodamine isothiocynate (RhIc). In rats receiving 2 or 3 injections of glucocorticoids and killed at the age of 4 or 7 days, between 40 to 60% of the callosal amoeboid microglial cells were depleted when compared with the corresponding control animals. The cells that survived the glucocorticoid treatments became ramified, while those in the controls of the same age group remained round or amoeboidic. In rats killed at 2 or 3 weeks of age, the microglia became extremely ramified with a concomitant diminution in their immunostaining, particularly in the glucocorticoid-injected rats. In rats receiving glucocorticoid injections along with RhIc, the RhIc-laden amoeboid microglia appeared round and amoeboidic and were intensely stained with OX-42, suggesting their activation and upregulation of complement type 3 receptors when compared with rats receiving only glucocorticoids. Compared with the control, cellular proliferation continued in rats given glucocorticoid injection as indicated by the occurrence of many bromodeoxyuridine-labelled cells in the corpus callosum at the age of 6 days. Ultrastructural studies confirmed the presence of mitotic cells identified as amoeboid microglia because of their labelling with isolectin. A striking ultrastructural feature in glucocorticoids-injected rats was the wide occurrence of amoeboid microglial cells that had ingested a variable number of lectin-labelled cells. It is concluded from this study that the drastic reduction of amoeboid microglia after glucocorticoid injections can be attributed to the suppression of their precursor cells, monocytes. Another possible explanation is the acceleration of their degeneration process, probably greatly enhanced by glucocorticoids; the degenerating amoeboid microglia were readily eliminated by the surviving amoeboid microglial cells through endocytosis. Glucocorticoids also accelerated the maturation process of the persisting amoeboid microglia to become ramified in form.
对出生后的大鼠进行皮下注射糖皮质激素，结果显示胼胝体中阿米巴样小胶质细胞数量急剧减少，这通过用OX系列单克隆抗体、ED1、凝集素和异硫氰酸罗丹明（RhIc）标记得以证实。在接受2或3次糖皮质激素注射并于4或7日龄处死的大鼠中，与相应的对照动物相比，胼胝体中40%至60%的阿米巴样小胶质细胞减少。在糖皮质激素处理后存活下来的细胞变成了分支状，而同龄对照组的细胞仍呈圆形或阿米巴样。在2或3周龄处死的大鼠中，小胶质细胞变得极度分支化，同时其免疫染色减弱，尤其是在注射糖皮质激素的大鼠中。在接受糖皮质激素注射并同时注射RhIc的大鼠中，负载RhIc的阿米巴样小胶质细胞呈圆形且阿米巴样，并被OX - 42强烈染色，这表明与仅接受糖皮质激素的大鼠相比，它们的补体3型受体被激活且上调。与对照组相比，注射糖皮质激素的大鼠中细胞增殖持续，这表现为在6日龄时胼胝体中有许多溴脱氧尿苷标记的细胞。超微结构研究证实了有丝分裂细胞的存在，这些细胞被鉴定为阿米巴样小胶质细胞，因为它们被异凝集素标记。注射糖皮质激素的大鼠中一个显著的超微结构特征是广泛存在摄取了不同数量凝集素标记细胞的阿米巴样小胶质细胞。从这项研究得出的结论是，糖皮质激素注射后阿米巴样小胶质细胞的急剧减少可归因于其前体细胞单核细胞的抑制。另一种可能的解释是它们的退化过程加速，这可能被糖皮质激素大大增强；退化的阿米巴样小胶质细胞很容易被存活的阿米巴样小胶质细胞通过内吞作用清除。糖皮质激素还加速了持续存在的阿米巴样小胶质细胞成熟为分支状的过程。
