Evidence map›Paper›PMID 17226020›Full record

ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2007

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

Frank Schuettauf, Sebastian Thaler, Sylvia Bolz, Julia Fries, Hubert Kalbacher, Anna Mankowska, David Zurakowski, Eberhart Zrenner, Robert Rejdak

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In one paragraph

Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Tryptophan Pathway Abnormalities in a Murine Model of Hereditary Glaucoma.International journal of molecular sciences · 2021
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  8. Loss of outer retinal neurons and circuitry alterations in the DBA/2J mouse.Investigative ophthalmology & visual science · 2014
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  18. K(+) currents fail to change in reactive retinal glial cells in a mouse model of glaucoma.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2008
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

Frank SchuettaufDepartment of Pathophysiology of Vision and Neuro-Ophthalmology, University Eye Hospital, Schleichstrasse 12, 72076 Tübingen, Germany. fschuettauf@uni-tuebingen.de
Sebastian Thaler
Sylvia Bolz
Julia Fries
Hubert Kalbacher
Anna Mankowska
David Zurakowski
Eberhart Zrenner
Robert Rejdak
STZ eyetrial · DEMedical University of Lublin · PLBoston Children's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe 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.

methodsRetinas 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.

resultsHPLC 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.

conclusionAlterations 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.

Indexed as

Amino AcidsAmino Acid Transport System X-AGAnimalsApoptosisAqueous HumorBlotting, WesternChromatography, High Pressure LiquidDisease Models, AnimalFemaleImmunoenzyme TechniquesMiceMice, Inbred C57BLMice, Inbred DBAOcular HypertensionReceptors, GlutamateRetinaAmino AcidsAmino Acid Transport System X-AGReceptors, Glutamate

Identifiers

PMID17226020
OpenAlexW2074041367

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.