Limited energy supply in Müller cells alters glutamate uptake.
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.
Department of Neuroscience and Pharmacology, the Panum Institute, University of Copenhagen, Blegdamsvej 3b, 2200, Copenhagen, Denmark.
Anne Katrine
AK
Toft-Kehler
Dorte Marie
DM
Skytt
Kristian Arild
KA
Poulsen
Charlotte Taul
CT
Brændstrup
Georgi
G
Gegelashvili
Helle
H
Waagepetersen
Miriam
M
Kolko
D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D026603:D-Aspartic Acid / Q000378:metabolism; D063928:Ependymoglial Cells / Q000502:physiology*; D027341:Excitatory Amino Acid Transporter 1 / Q000378:metabolism; D027342:Excitatory Amino Acid Transporter 2 / Q000378:metabolism; D005947:Glucose / Q000172:deficiency*; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D015854:Up-Regulation
D027341:Excitatory Amino Acid Transporter 1; D027342:Excitatory Amino Acid Transporter 2; D018698:Glutamic Acid; D026603:D-Aspartic Acid; D005947:Glucose