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Alterations of amino acids and glutamate transport in the DBA/2J mouse retina; possible clues to degeneration

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Alterations of amino acids and glutamate transport in the DBA/2J mouse retina; possible clues to degeneration. / Schuettauf, Frank; Thaler, Sebastian; Bolz, Sylvia; Fries, Julia; Kalbacher, Hubert; Mankowska, Anna; Zurakowski, David; Zrenner, Eberhart; Rejdak, Robert.

in: GRAEF ARCH CLIN EXP, Jahrgang 245, Nr. 8, 08.2007, S. 1157-68.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Schuettauf, F, Thaler, S, Bolz, S, Fries, J, Kalbacher, H, Mankowska, A, Zurakowski, D, Zrenner, E & Rejdak, R 2007, 'Alterations of amino acids and glutamate transport in the DBA/2J mouse retina; possible clues to degeneration', GRAEF ARCH CLIN EXP, Jg. 245, Nr. 8, S. 1157-68. https://doi.org/10.1007/s00417-006-0531-z

APA

Schuettauf, F., Thaler, S., Bolz, S., Fries, J., Kalbacher, H., Mankowska, A., Zurakowski, D., Zrenner, E., & Rejdak, R. (2007). Alterations of amino acids and glutamate transport in the DBA/2J mouse retina; possible clues to degeneration. GRAEF ARCH CLIN EXP, 245(8), 1157-68. https://doi.org/10.1007/s00417-006-0531-z

Vancouver

Schuettauf F, Thaler S, Bolz S, Fries J, Kalbacher H, Mankowska A et al. Alterations of amino acids and glutamate transport in the DBA/2J mouse retina; possible clues to degeneration. GRAEF ARCH CLIN EXP. 2007 Aug;245(8):1157-68. https://doi.org/10.1007/s00417-006-0531-z

Bibtex

@article{60c3a387e6654843a68262247d8dfdbb,
title = "Alterations of amino acids and glutamate transport in the DBA/2J mouse retina; possible clues to degeneration",
abstract = "BACKGROUND: The DBA/2J mouse spontaneously develops ocular hypertension and time-dependent progressive retinal ganglion cell (RGC) loss. This study examines changes in amino acid levels in the vitreous, and changes in the expression of retinal glutamate transporters and receptors that occur during the progression of this pathology.METHODS: Retinas were obtained from DBA/2J mice at ages 3, 6 and 11 months. C57BL/6 mice were used as age-matched controls. Vitreal amino acid content was measured with HPLC. Western blotting and immunohistochemistry were performed using specific antibodies against the glutamate transporters (GLAST, GLT-1v, EAAC-1) and glutamate receptors, particularly NMDA (NR1, NR2A, NR2B) and AMPA (GluR1, GluR2/3, GluR4) receptors.RESULTS: HPLC showed retinal concentrations of glutamate, glutamine, glycine, alanine, lysine, serine, and arginine to be significantly higher in DBA/2J mice at 11 months of age compared to age-matched controls. Western Blots revealed a moderate decrease of GLAST and GLT-1v expression in DBA/2J mice at 6 and 11 months as compared to age-matched controls while there was no change in EAAC1. Immunohistochemically, no changes in expression of NMDA and AMPA receptors were seen.CONCLUSION: Alterations of amino acid content and enhanced glutamate neurotransmission might be involved in the pathogenesis of retinal neurodegeneration in the DBA/ 2J mouse model of ocular hypertension. Moreover, these mice provide an animal model for studying excitotoxic retinal damage.",
keywords = "Amino Acid Transport System X-AG/metabolism, Amino Acids/metabolism, Animals, Apoptosis, Aqueous Humor/metabolism, Blotting, Western, Chromatography, High Pressure Liquid, Disease Models, Animal, Female, Immunoenzyme Techniques, Mice, Mice, Inbred C57BL, Mice, Inbred DBA, Ocular Hypertension/metabolism, Receptors, Glutamate/metabolism, Retina/metabolism, Retinal Degeneration/metabolism, Retinal Ganglion Cells/metabolism",
author = "Frank Schuettauf and Sebastian Thaler and Sylvia Bolz and Julia Fries and Hubert Kalbacher and Anna Mankowska and David Zurakowski and Eberhart Zrenner and Robert Rejdak",
year = "2007",
month = aug,
doi = "10.1007/s00417-006-0531-z",
language = "English",
volume = "245",
pages = "1157--68",
journal = "GRAEF ARCH CLIN EXP",
issn = "0721-832X",
publisher = "Springer",
number = "8",

}

RIS

TY - JOUR

T1 - Alterations of amino acids and glutamate transport in the DBA/2J mouse retina; possible clues to degeneration

AU - Schuettauf, Frank

AU - Thaler, Sebastian

AU - Bolz, Sylvia

AU - Fries, Julia

AU - Kalbacher, Hubert

AU - Mankowska, Anna

AU - Zurakowski, David

AU - Zrenner, Eberhart

AU - Rejdak, Robert

PY - 2007/8

Y1 - 2007/8

N2 - BACKGROUND: The DBA/2J mouse spontaneously develops ocular hypertension and time-dependent progressive retinal ganglion cell (RGC) loss. This study examines changes in amino acid levels in the vitreous, and changes in the expression of retinal glutamate transporters and receptors that occur during the progression of this pathology.METHODS: Retinas were obtained from DBA/2J mice at ages 3, 6 and 11 months. C57BL/6 mice were used as age-matched controls. Vitreal amino acid content was measured with HPLC. Western blotting and immunohistochemistry were performed using specific antibodies against the glutamate transporters (GLAST, GLT-1v, EAAC-1) and glutamate receptors, particularly NMDA (NR1, NR2A, NR2B) and AMPA (GluR1, GluR2/3, GluR4) receptors.RESULTS: HPLC showed retinal concentrations of glutamate, glutamine, glycine, alanine, lysine, serine, and arginine to be significantly higher in DBA/2J mice at 11 months of age compared to age-matched controls. Western Blots revealed a moderate decrease of GLAST and GLT-1v expression in DBA/2J mice at 6 and 11 months as compared to age-matched controls while there was no change in EAAC1. Immunohistochemically, no changes in expression of NMDA and AMPA receptors were seen.CONCLUSION: Alterations of amino acid content and enhanced glutamate neurotransmission might be involved in the pathogenesis of retinal neurodegeneration in the DBA/ 2J mouse model of ocular hypertension. Moreover, these mice provide an animal model for studying excitotoxic retinal damage.

AB - BACKGROUND: The DBA/2J mouse spontaneously develops ocular hypertension and time-dependent progressive retinal ganglion cell (RGC) loss. This study examines changes in amino acid levels in the vitreous, and changes in the expression of retinal glutamate transporters and receptors that occur during the progression of this pathology.METHODS: Retinas were obtained from DBA/2J mice at ages 3, 6 and 11 months. C57BL/6 mice were used as age-matched controls. Vitreal amino acid content was measured with HPLC. Western blotting and immunohistochemistry were performed using specific antibodies against the glutamate transporters (GLAST, GLT-1v, EAAC-1) and glutamate receptors, particularly NMDA (NR1, NR2A, NR2B) and AMPA (GluR1, GluR2/3, GluR4) receptors.RESULTS: HPLC showed retinal concentrations of glutamate, glutamine, glycine, alanine, lysine, serine, and arginine to be significantly higher in DBA/2J mice at 11 months of age compared to age-matched controls. Western Blots revealed a moderate decrease of GLAST and GLT-1v expression in DBA/2J mice at 6 and 11 months as compared to age-matched controls while there was no change in EAAC1. Immunohistochemically, no changes in expression of NMDA and AMPA receptors were seen.CONCLUSION: Alterations of amino acid content and enhanced glutamate neurotransmission might be involved in the pathogenesis of retinal neurodegeneration in the DBA/ 2J mouse model of ocular hypertension. Moreover, these mice provide an animal model for studying excitotoxic retinal damage.

KW - Amino Acid Transport System X-AG/metabolism

KW - Amino Acids/metabolism

KW - Animals

KW - Apoptosis

KW - Aqueous Humor/metabolism

KW - Blotting, Western

KW - Chromatography, High Pressure Liquid

KW - Disease Models, Animal

KW - Female

KW - Immunoenzyme Techniques

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Inbred DBA

KW - Ocular Hypertension/metabolism

KW - Receptors, Glutamate/metabolism

KW - Retina/metabolism

KW - Retinal Degeneration/metabolism

KW - Retinal Ganglion Cells/metabolism

U2 - 10.1007/s00417-006-0531-z

DO - 10.1007/s00417-006-0531-z

M3 - SCORING: Journal article

C2 - 17226020

VL - 245

SP - 1157

EP - 1168

JO - GRAEF ARCH CLIN EXP

JF - GRAEF ARCH CLIN EXP

SN - 0721-832X

IS - 8

ER -