Limited Energy Supply in Müller Cells Alters Glutamate Uptake
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The viability of retinal ganglion cells (RGC) is essential for the maintenance of visual function. RGC homeostasis is maintained by the surrounding retinal glial cells, the Müller cells, which buffer the extracellular concentration of neurotransmitters and provide the RGCs with energy. This study evaluates if glucose-deprivation of Müller cells interferes with their ability to remove glutamate from the extracellular space. The human Müller glial cell line, Moorfields/Institute of Ophthalmology-Müller 1, was used to study changes in glutamate uptake. Excitatory amino acid transporter (EAAT) proteins were up-regulated in glucose-deprived Müller cells and glutamate uptake was significantly increased in the absence of glucose. The present findings revealed an up-regulation of EAAT1 and EAAT2 in glucose-deprived Müller cells as well as an increased ability to take up glutamate. Hence, glucose deprivation may result in an increased ability to protect RGCs from glutamate-induced excitotoxicity, whereas malfunction of glutamate uptake in Müller cells may contribute to retinal neurodegeneration.
KeywordsGlutamate excitotoxicity EAAT Müller cells Retinal ganglion cells Neuroprotection
The authors thank technician Maja Udsen, Department of International Health, Immunology and Microbiology, University of Copenhagen, Denmark for skillful assistance to the study and Dr. Anna Rodriquez-Kern for EAAT-antibodies. The study was supported by The Danish Eye Health Society, The Danish Medical Research Council (Grant no. 0602-02113B) and The Lundbeck Foundation (Grant no. R88-A9077-B1012).
Conflict of interest
The authors declare that they have no conflict of interest.
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