Zeng X X, Ng Y K, Ling E A
Department of Anatomy, Faculty of Medicine, National University of Singapore, Singapore.
Vis Neurosci. 2000 May-Jun;17(3):463-71. doi: 10.1017/s0952523800173122.
This study reports Müller cell and neuronal changes and microglial reaction in streptozotocin-induced diabetic rats. Glial fibrillary acidic protein (GFAP) immunoreactivity was largely confined to astrocytes in the nerve fiber layer (NFL) and ganglion cell layer (GCL) in control rats. In diabetic rats especially those killed after 12 months, GFAP immunostaining could be traced along the entire length of Müller cell processes, extending from the inner to the outer limiting membrane. With the antibody neuronal nuclei, immunopositive cells were located in the GCL and the inner part of the inner nuclear layer (INL) in both diabetic and age-matched control rats. In diabetic rats, labelled cells were reduced in both layers being more marked in the INL. In age-matched control rats, OX42-immunoreactive microglial cells were distributed mainly in the NFL and GCL; some cells were localized in the inner plexiform layer, but rarely in the outer plexiform layer (OPL). Beginning 1 month after diabetes, the microglial cells appeared hypertrophic. Furthermore, microglial number as estimated from cell counts in different layers of the retina was significantly increased, with the occurrence of some cells in the OPL at 4 months. At 14 and 16 months, reactive microglial cells were detected in the outer nuclear layer and photoreceptor layer. Present results suggest that microglial reaction in induced diabetes was elicited by neuronal cell loss in both GCL and INL as well as by some pathologic changes affecting the photoreceptors.
本研究报告了链脲佐菌素诱导的糖尿病大鼠中 Müller 细胞、神经元的变化以及小胶质细胞反应。在对照大鼠中，胶质纤维酸性蛋白（GFAP）免疫反应主要局限于神经纤维层（NFL）和神经节细胞层（GCL）的星形胶质细胞。在糖尿病大鼠中，尤其是在 12 个月后处死的大鼠，GFAP 免疫染色可沿着 Müller 细胞突起的全长追踪到，从内界膜延伸至外界膜。使用神经元细胞核抗体，免疫阳性细胞在糖尿病大鼠和年龄匹配的对照大鼠的 GCL 和内核层（INL）内部均有定位。在糖尿病大鼠中，两层中的标记细胞均减少，在 INL 中更为明显。在年龄匹配的对照大鼠中，OX42 免疫反应性小胶质细胞主要分布在 NFL 和 GCL；一些细胞位于内网状层，但很少在外网状层（OPL）。糖尿病开始 1 个月后，小胶质细胞出现肥大。此外，根据视网膜不同层的细胞计数估计，小胶质细胞数量显著增加，4 个月时 OPL 出现一些细胞。在 14 个月和 16 个月时，在外核层和光感受器层检测到反应性小胶质细胞。目前的结果表明，诱导性糖尿病中的小胶质细胞反应是由 GCL 和 INL 中的神经元细胞丢失以及影响光感受器的一些病理变化引起的。
