Evidence map›Paper›PMID 15688208›Full record

ArticleDiabetologia2005

Glutamate uptake in retinal glial cells during diabetes.

M M Ward, A I Jobling, M Kalloniatis, E L Fletcher

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 74 citations in OpenAlex.

  1. Case series: The role of retinal ischemia in the pathogenesis and clinical manifestation of diabetic retinopathy.Optometry and vision science : official publication of the American Academy of Optometry · 2026
    Article
  2. Neuroprotection in Early Diabetic Retinal Disease Using Eyedrop Delivery.International journal of molecular sciences · 2026
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  14. Role of interleukin-1β in hypoxia-induced depression of glutamate uptake in retinal Müller cells.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2014
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  19. Nuclear GAPDH: changing the fate of Müller cells in diabetes.Journal of ocular biology, diseases, and informatics · 2011
    Article
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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

4 authors at 2 institutions in 2 countries.

M M WardDepartment of Anatomy and Cell Biology, The University of Melbourne, Grattan St, Parkville, 3010 Victoria, Australia.
A I Jobling
M Kalloniatis
E L Fletcher
University of Melbourne · AUUniversity of Auckland · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsGlutamate recycling is a major function of retinal Muller cells. The aim of this study was to evaluate the expression and function of glutamate transporters during diabetes.

methodsSprague-Dawley rats were rendered diabetic by a single dose of streptozotocin (50 mg/kg). Following 12 weeks of diabetes, immunolocalisation and mRNA expression of the two glial cell transporters, GLAST and EAAT4 were evaluated using indirect immunofluorescence and real-time PCR. The function of glutamate transport was investigated at 1, 4 and 12 weeks following induction of diabetes by measuring the level of uptake of the non-metabolisable glutamate analogue, D: -aspartate, into Muller cells.

resultsThere was no difference in the localisation of either GLAST or EAAT4 during diabetes. Although there was a small apparent increase in expression of both GLAST and EAAT4 in diabetic retinae compared with controls this was not statistically significant. At 1, 4 and 12 weeks following diabetes, D: -aspartate immunoreactivity was significantly increased in Muller cells of diabetic rats compared to controls (p<0.001). The EC(50) was found to increase by 0.304 log units in diabetic Muller cells compared with controls, suggesting that glutamate uptake is twice as efficient.

conclusionsThese data suggest that there are alterations in glutamate transport during diabetes. However, these changes are unlikely to play a significant role in glutamate-induced neuronal excitoxicity during diabetes. These results suggest that although Muller cells undergo gliosis at an early stage of diabetes, one of the most important functions for maintaining normal retinal function is preserved within the retina.

Indexed as

Amino Acid Transport System X-AGAnimalsBlood GlucoseDiabetes Mellitus, ExperimentalExcitatory Amino Acid Transporter 1Excitatory Amino Acid Transporter 4Glutamate Plasma Membrane Transport ProteinsGlutamic AcidMaleRatsRats, Sprague-DawleyReference ValuesRetinaRetinal Ganglion CellsReverse Transcriptase Polymerase Chain ReactionRNA, MessengerAmino Acid Transport System X-AGBlood GlucoseExcitatory Amino Acid Transporter 1Excitatory Amino Acid Transporter 4Glutamate Plasma Membrane Transport ProteinsGlutamic AcidRNA, MessengerSlc1a3 protein, ratSlc1a6 protein, ratSymporters

Identifiers

PMID15688208
OpenAlexW2052513767

What OpenQuestion holds

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Registered trials

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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.