Rats After Acute High Intraocular Pressure, Retinal Glutamine Synthetase Expression Changes

Glaucoma is one of the main reasons of blindness, which mainly results from intraocular hypertension and ischemia and is characterized by optic nerve injury and loss of retinal ganglion cells(RGCs). Lots of investigations suggested that loss of RGCs is involed in excitoxicity of glutamate. However, expression and function of glutamine synthetase, one of main metabolic enzyme of glutamate, is still not reported in the glaucomatous retina. Here we detected the expression of glutamate synthetase(GS) in the rat retina following acute intraocular hypertension(AIH). The intraocular pressure of the left eyes of 48 wistar rats was raised to the threshold value equal to the pressure needed to make the b wave of electroretinogram disappear. The intact right eyes served as controls. The animals were sacrificed either immediately(Od) or 1,3,7 or 14 days post-AIH. Immunocytochemistry and Western blot analysis were used to examine the changes of GS expression. Our results showed that GS-ir was mainly localized in the Muller cell body in the normal retinas. Following AIH, bands of GS-ir were shown in the inner plexiform layer( IPL) of 0-d retina with mild decrease in the Muller cell bodies, followed by the intense and diffuse staining in IPL of 1-d and 3-d groups. By contrast, the 7-d and 14-d groups resembled the controls. During the process, there were not obvious changes of staining around the vesicles in ganglion cell layer. Western blot analysis of retina from normal and AIH eyes showed GS as a single protein band with a molecular weight of 45 kDa. Quantitatively, GS protein level increased in the 1-d group and then decreased gradually to control by day 14. The redistribution and up-regulation of GS may suggest that GS improves the metabolism of extracellular glutamate and then protects the retina, especially ganglion cells, following AIH...