Limited energy supply in Müller cells alters glutamate uptake

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

doi:10.1007/s11064-014-1289-z

Limited energy supply in Müller cells alters glutamate uptake

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

18 Citations (Scopus)

Abstract

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 language	English
Journal	Neurochemical Research
Volume	39
Issue number	5
Pages (from-to)	941-9
Number of pages	9
ISSN	0364-3190
DOIs	https://doi.org/10.1007/s11064-014-1289-z
Publication status	Published - May 2014

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title = "Limited energy supply in M{\"u}ller cells alters glutamate uptake",

abstract = "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 M{\"u}ller cells, which buffer the extracellular concentration of neurotransmitters and provide the RGCs with energy. This study evaluates if glucose-deprivation of M{\"u}ller cells interferes with their ability to remove glutamate from the extracellular space. The human M{\"u}ller glial cell line, Moorfields/Institute of Ophthalmology-M{\"u}ller 1, was used to study changes in glutamate uptake. Excitatory amino acid transporter (EAAT) proteins were up-regulated in glucose-deprived M{\"u}ller 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 M{\"u}ller 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 M{\"u}ller cells may contribute to retinal neurodegeneration.",

author = "Toft-Kehler, {Anne Katrine} and Skytt, {Dorte Marie} and Poulsen, {Kristian Arild} and Br{\ae}ndstrup, {Charlotte Taul} and Georgi Gegelashvili and Waagepetersen, {Helle S.} and Miriam Kolko",

year = "2014",

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doi = "10.1007/s11064-014-1289-z",

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T1 - Limited energy supply in Müller cells alters glutamate uptake

AU - Toft-Kehler, Anne Katrine

AU - Skytt, Dorte Marie

AU - Poulsen, Kristian Arild

AU - Brændstrup, Charlotte Taul

AU - Gegelashvili, Georgi

AU - Waagepetersen, Helle S.

AU - Kolko, Miriam

PY - 2014/5

Y1 - 2014/5

N2 - 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.

AB - 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.

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DO - 10.1007/s11064-014-1289-z

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VL - 39

SP - 941

EP - 949

JO - Neurochemical Research

JF - Neurochemical Research

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ER -

Limited energy supply in Müller cells alters glutamate uptake

Abstract

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