Diabetes-induced dysfunction of retinal Müller cells.

Abstract

Soon after the onset of experimental diabetes, the function of the glutamate transporter in Müller cells is decreased by a mechanism that is likely to involve oxidation. The demonstration that the activity of this transporter can be rapidly restored raises the possibility that targeting this molecule for therapeutic intervention may restore glutamate homeostasis and, thereby, ameliorate sight-threatening complications of diabetic retinopathy.