Evidence map›Paper›PMID 19535601›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Regulation of glutamate transport in developing rat oligodendrocytes.

Tara M DeSilva, Anatoli Y Kabakov, Patricia E Goldhoff, Joseph J Volpe, Paul A Rosenberg

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

43 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
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  6. Blockade of L-Type CaCurrent issues in molecular biology · 2023
    Article
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  15. Review
  16. Article
  17. Glutamate Transport and Preterm Brain Injury.Frontiers in physiology · 2019
    Review
  18. Article
  19. 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

5 authors at 3 institutions in 1 country.

Tara M DeSilvaDepartment of Neurology and F. M. Kirby Neurobiology Center, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Anatoli Y Kabakov
Patricia E Goldhoff
Joseph J Volpe
Paul A Rosenberg
Harvard University · USBoston Children's Hospital · USHarvard University Press · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI CHEN, CHINFEI · 1985 to 2015
$26.2M
PERIVENTRICULAR LEUKOMALACIA IN THE PREMATURE INFANTP01NS038475 · NINDS · CHILDREN'S HOSPITAL BOSTON · PI VOLPE, JOSEPH J · 2000 to 2009
$13.2M
EXPRESSION OF EAAT2 IN THE DEVELOPING HUMAN BRAINR01NS041883 · NINDS · CHILDREN'S HOSPITAL BOSTON · PI ROSENBERG, PAUL ALLEN · 2000 to 2004
$1.6M
GLUTAMATE TRANSPORT AND TRANSPORTERS FOREBRIAN NEURONSR01NS040753 · NINDS · CHILDREN'S HOSPITAL BOSTON · PI ROSENBERG, PAUL ALLEN · 2001 to 2004
$1.2M
NICHD NIH HHS HD18655NICHD NIH HHS P30 HD018655NINDS NIH HHS NS38475NINDS NIH HHS NS40753NINDS NIH HHS NS41883NINDS NIH HHS P01 NS038475NINDS NIH HHS R01 NS040753NINDS NIH HHS R01 NS041883
6 · The paper itself

Abstract

Glutamate released from synaptic vesicles mediates excitatory neurotransmission by stimulating glutamate receptors. Glutamate transporters maintain low synaptic glutamate levels critical for this process, a role primarily attributed to astrocytes. Recently, vesicular release of glutamate from unmyelinated axons in the rat corpus callosum has been shown to elicit AMPA receptor-mediated currents in glial progenitor cells. Glutamate transporters are the only mechanism of glutamate clearance, yet very little is known about the role of glutamate transporters in normal development of oligodendrocytes (OLs) or in excitotoxic injury to OLs. We found that OLs in culture are capable of sodium-dependent glutamate uptake with a K(m) of 10 +/- 2 microm and a V(max) of 2.6, 5.0, and 3.8 nmol x min(-1) x mg(-1) for preoligodendrocytes, immature, and mature OLs, respectively. Surprisingly, EAAC1, thought to be exclusively a neuronal transporter, contributes more to [(3)H]l-glutamate uptake in OLs than GLT1 or GLAST. These data suggest that glutamate transporters on oligodendrocytes may serve a critical role in maintaining glutamate homeostasis at a time when unmyelinated callosal axons are engaging in glutamatergic signaling with glial progenitors. Furthermore, GLT1 was significantly increased in cultured mature OLs contrary to in vivo data in which we have shown that, although GLT1 is present on developing OLs when unmyelinated axons are prevalent in the developing rat corpus callosum, after myelination, GLT1 is not expressed on mature OLs. The absence of GLT1 in mature OLs in the rat corpus callosum and its presence in mature rat cultured OLs may indicate that a signaling process in vivo is not activated in vitro.

Indexed as

AnimalsAnimals, NewbornAspartic AcidBenzodiazepinesBicucullineBrainCells, CulturedExcitatory Amino Acid AntagonistsExcitatory Amino Acid Transporter 2Excitatory Amino Acid Transporter 3FemaleFibroblast Growth FactorsGABA AntagonistsGangliosidesGene Expression Regulation, DevelopmentalGlutamic Acid2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxalineAspartic AcidBenzodiazepinesbenzyloxyaspartateBicucullinedihydrokainic acidExcitatory Amino Acid AntagonistsExcitatory Amino Acid Transporter 2Excitatory Amino Acid Transporter 3Fibroblast Growth FactorsGABA Antagonistsganglioside A2B5GangliosidesGlutamic AcidGYKI 52466Kainic AcidO AntigensPlatelet-Derived Growth FactorQuinoxalinesSlc1a1 protein, ratSodium Channel BlockersTetrodotoxinTritium

Identifiers

PMID19535601
PMCPMC2926807
OpenAlexW2089249713

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.