Limited energy supply in Müller cells alters glutamate uptake

Research output: Contribution to journalJournal articleResearchpeer-review

Anne Katrine Toft-Kehler, Dorte Marie Skytt, Kristian Arild Poulsen, Charlotte Taul Brændstrup, Georgi Gegelashvili, Helle S. Waagepetersen, Miriam Kolko

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.

Original languageEnglish
JournalNeurochemical Research
Volume39
Issue number5
Pages (from-to)941-9
Number of pages9
ISSN0364-3190
DOIs
Publication statusPublished - May 2014

ID: 120585430