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Korean J Anat. 2002 Aug;35(4):315-324. Korean. Original Article.
Park SH , Park JW , Chung JW , Chun MH , Oh SJ .
Department of Anatomy, College of Medicine, The Catholic University of Korea, Seoul, Korea. sujaoh@catholic.ac.kr
Abstract

Diabetic hyperglycemia induces transient ischemia in the neural retina. High level of extracellular glutamate resulting from ischemia, in turn, influences on glutamate homeostasis. The present study has been conducted to clarify the alteration of the glutamate homeostasis-associated substances in the retinal Muller cells in response to a diabetic injury by streptozotocin injection. Young adult Sprague -Dawley rats were injected with streptozotocin (60 mg/kg body weight in 0.05 M sodium citrate buffer, pH 5.5) under anesthesia with 4% chloral hydrate. Animals above 300 mg/dl in blood glucose level were cared for 1, 4, 12 and 24 weeks, respectively. At each time-point, the retinas were dissected out and processed for immuno-histochemical and immunoblotting analyses by using guinea pig anti -GLAST and mouse anti-glutamine synthetase (GS) antibodies. In the normal retina, GLAST and GS were immuno-localized in the Muller cells, the outer plexiform layer (OPL), the border between the inner nuclear layer and the inner plexiform layer (IPL), a band in the middle of the IPL, and the border between the IPL and the ganglion cell layer. The expression of both proteins was decreased remarkably in the OPL by 12 weeks of diabetes and increased slightly in the end feet of the Muller cells from 4 weeks onwards. Immunoblotting results of the two proteins in the diabetic retinas were largely consistent with those of immuno-histochemistry. These results suggest that the alteration of glutamate homeostasis in the diabetic state is initiated mainly in the OPL by decreasing the uptake of glutamate via down-regulated GLAST.

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