Evidence map›Paper›PMID 19188250›Full record

ArticleThe Journal of physiology2009

Bradykinin-induced astrocyte-neuron signalling: glutamate release is mediated by ROS-activated volume-sensitive outwardly rectifying anion channels.

Hong-Tao Liu, Tenpei Akita, Takahiro Shimizu, Ravshan Z Sabirov, Yasunobu Okada

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

62 citing papers in PubMed, 104 citations in OpenAlex.

  1. Article
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  17. NMDARs, Coincidence Detectors of Astrocytic and Neuronal Activities.International journal of molecular sciences · 2021
    Review
  18. Review
  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

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 2 countries.

Hong-Tao LiuDepartment of Cell Physiology, National Institute for Physiological Sciences, 38 Nishigonaka, Myodaiji-cho, Okazaki, Aichi 444-8585, Japan.
Tenpei Akita
Takahiro Shimizu
Ravshan Z Sabirov
Yasunobu Okada
National Institutes of Natural Sciences · JPFirst Hospital of China Medical University · CNNational Institute for Physiological Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glial cells release gliotransmitters which signal to adjacent neurons and glial cells. Previous studies showed that in response to stimulation with bradykinin, glutamate is released from rat astrocytes and causes NMDA receptor-mediated elevation of intracellular Ca(2+) in adjacent neurons. Here, we investigate how bradykinin-induced glutamate release from mouse astrocytes signals to neighbouring neurons in co-cultures. Astrocyte-to-neuron signalling and bradykinin-induced glutamate release from mouse astrocytes were both inhibited by the anion channel blocker 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) and phloretin. Glutamate release was also sensitive to 4-(2-Butyl-6,7-dichlor-2-cyclopentylindan-1-on-5-yl) oxybutyric acid (DCPIB), a specific blocker of the volume-sensitive outwardly rectifying anion channel (VSOR). Astrocytes, but not neurons, responded to bradykinin with activation of whole-cell Cl- currents. Although astrocytes stimulated with bradykinin did not undergo cell swelling, the bradykinin-activated current exhibited properties typical of VSOR: outward rectification, inhibition by osmotic shrinkage, sensitivity to DIDS, phloretin and DCPIB, dependence on intracellular ATP, and permeability to glutamate. Bradykinin increased intracellular reactive oxygen species (ROS) in mouse astrocytes. Pretreatment of mouse astrocytes with either a ROS scavenger or an NAD(P)H oxidase inhibitor blocked bradykinin-induced activation of VSOR, glutamate release and astrocyte-to-neuron signalling. By contrast, pretreatment with BAPTA-AM or tetanus neurotoxin A failed to suppress bradykinin-induced glutamate release. Thus, VSOR activated by ROS in mouse astrocytes in response to stimulation with bradykinin, serves as the pathway for glutamate release to mediate astrocyte-to-neuron signalling. Since bradykinin is an initial mediator of inflammation, VSOR might play a role in glia-neuron communication in the brain during inflammation.

Indexed as

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic AcidAnimalsAstrocytesBradykininBradykinin Receptor AntagonistsCalcium SignalingCell ShapeCerebral CortexCoculture TechniquesElectric StimulationEnzyme InhibitorsFree Radical ScavengersGlutamic AcidHypertonic SolutionsHypotonic SolutionsIon Channels4,4'-Diisothiocyanostilbene-2,2'-Disulfonic AcidBradykininBradykinin Receptor AntagonistsEnzyme InhibitorsFree Radical ScavengersGlutamic AcidHypertonic SolutionsHypotonic SolutionsIon ChannelsNADH, NADPH OxidoreductasesPhloretinReactive Oxygen SpeciesReceptors, N-Methyl-D-Aspartate

Identifiers

PMID19188250
PMCPMC2697293
OpenAlexW1602049707

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.