Evidence map›Paper›PMID 15254085›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Glutamate transporter cluster formation in astrocytic processes regulates glutamate uptake activity.

Jianzheng Zhou, Margaret L Sutherland

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

57 citing papers in PubMed, 116 citations in OpenAlex.

  1. Review
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  4. Pathological phenotypes of astrocytes in Alzheimer's disease.Experimental & molecular medicine · 2024
    Review
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  19. The neuroprotective mechanism of ampicillin in a mouse model of transient forebrain ischemia.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016
    Article
  20. 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

2 authors at 1 institution in 1 country.

Jianzheng ZhouDepartment of Pharmacology, The George Washington University, Washington, DC 20037, USA.
Margaret L Sutherland
George Washington University · US

Funding

Investigating a Role for Glutamate Transport in EpilepsyR01NS042854 · NINDS · GEORGE WASHINGTON UNIVERSITY · PI SUTHERLAND, MARGARET L · 2002 to 2006
$1.5M
Neuroprotective Properties of Enhanced Glutamate UptakeR01NS041679 · NINDS · GEORGE WASHINGTON UNIVERSITY · PI SUTHERLAND, MARGARET L · 2001 to 2005
$1.4M
NINDS NIH HHS NS41679NINDS NIH HHS NS42854NINDS NIH HHS R01 NS041679NINDS NIH HHS R01 NS042854
6 · The paper itself

Abstract

Glutamate is the predominant excitatory neurotransmitter in the CNS, and it is removed from the synaptic cleft by sodium-dependent glutamate transport activity. Glutamate transporter-1 (GLT-1) is expressed predominantly in astroglial cells and is responsible for the largest proportion of glutamate transport in the adult forebrain. In the present study, we demonstrate the ability of endogenous and recombinant GLT-1 to form clusters in astrocytic processes and characterize the mobility and physiological importance of these clusters in the regulation of GLT-1 activity in the presence or absence of neurons. At the distal end of C6 glioma cell processes, GLT-1 clusters undergo rapid morphological changes in both shape and size, and these changes are inhibited by cytochalasin D treatment, suggesting that the morphogenesis of GLT-1 clusters is highly dependent on the actin network. Treatment of astrocytes with phorbol 12-myristate 13-acetate (PMA) quickly and preferentially decreases GLT-1 localization on the process membrane, leading to de novo generation of GLT-1 clusters along the process shaft. Pretreatment with the PKC inhibitor bisindolylmaleimide II (Bis II), with sucrose (0.4 m), or through the expression of a dominant-negative form of dynamin prevents PMA-induced GLT-1 internalization and cluster formation. In terms of glutamate transporter function, PMA treatment elicits a significant decrease in GLT-1 activity that is prevented by preexposure to either Bis II or hypertonic treatment. Together, these data indicate that GLT-1 trafficking and cluster formation in glial cell processes are dynamic events that play important roles in regulating glutamate uptake in astrocytes and glioma cells.

Indexed as

Actin CytoskeletonActinsAnimalsAstrocytesBrain NeoplasmsCell CompartmentationCell Line, TumorCell Surface ExtensionsExcitatory Amino Acid Transporter 2GliomaGlutamic AcidGreen Fluorescent ProteinsMiceProtein TransportRecombinant Fusion ProteinsSucroseActinsExcitatory Amino Acid Transporter 2Glutamic AcidGreen Fluorescent ProteinsRecombinant Fusion ProteinsSucroseTetradecanoylphorbol Acetate

Identifiers

PMID15254085
PMCPMC6729534
OpenAlexW1884333838

What OpenQuestion holds

Textmetadata
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.