Limited energy supply in Müller cells alters glutamate uptake
| Autor: | Kristian Arild Poulsen, Georgi Gegelashvili, Dorte M. Skytt, Charlotte Taul Brændstrup, Helle S. Waagepetersen, Anne Katrine Toft-Kehler, Miriam Kolko |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
Cell Survival
Ependymoglial Cells Excitotoxicity Glutamic Acid Biology medicine.disease_cause Biochemistry Neuroprotection Retinal ganglion Cell Line Cellular and Molecular Neuroscience chemistry.chemical_compound Extracellular medicine Humans D-Aspartic Acid Glutamate receptor Retinal General Medicine Cell biology Up-Regulation Excitatory Amino Acid Transporter 1 Glucose chemistry Excitatory Amino Acid Transporter 2 Cell culture sense organs Homeostasis |
| Zdroj: | Neurochemical research. 39(5) |
| ISSN: | 1573-6903 |
| Popis: | 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 Muller cells, which buffer the extracellular concentration of neurotransmitters and provide the RGCs with energy. This study evaluates if glucose-deprivation of Muller cells interferes with their ability to remove glutamate from the extracellular space. The human Muller glial cell line, Moorfields/Institute of Ophthalmology-Muller 1, was used to study changes in glutamate uptake. Excitatory amino acid transporter (EAAT) proteins were up-regulated in glucose-deprived Muller 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 Muller 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 Muller cells may contribute to retinal neurodegeneration. |
| Databáze: | OpenAIRE |
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