Neuronal and microglial response in the retina of streptozotocin-induced diabetic rats

This study reports Muller 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 fibe r layer (NFL) and ganglion cell layer (GCL) in control rats. In diabetic ra ts especially those killed after 12 months, GFAP immunostaining could be tr aced along the entire length of Muller cell processes, extending from the i nner to the outer limiting membrane. With the antibody neuronal nuclei, imm unopositive cells were located in the GCL and the inner part of the inner n uclear layer (INL) in both diabetic and age-matched control mts. In diabeti c rats, labelled cells were reduced in both layers being more marked in the INL. In age-matched control rats, OX42-immunoreactive microglial cells wer e distributed mainly in the NFL and GCL; some cells were localized in the i nner plexiform layer, but rarely in the outer plexiform layer (OPL). Beginn ing 1 month after diabetes, the microglial cells appeared hypertrophic. Fur thermore, microglial number as estimated from cell counts in different laye rs of the retina was significantly increased, with the occurrence of some c ells in the OPL at 4 months. At 14 and 16 months, reactive microglial calls were detected in the outer nuclear layer and photoreceptor layer. Present results suggest that microglial reaction in induced diabetes was elicited b y neuronal cell loss in both GCL and INL as well as by some pathologic chan ges affecting the photoreceptors.