Evidence map›Paper›PMID 16527858›Full record

ArticleThe Journal of physiology2006

Pharmacological comparison of swelling-activated excitatory amino acid release and Cl- currents in cultured rat astrocytes.

Iskandar F Abdullaev, Alena Rudkouskaya, Gary P Schools, Harold K Kimelberg, Alexander A Mongin

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
3.9field-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

80 citing papers in PubMed, 126 citations in OpenAlex.

  1. Article
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  8. Review
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  16. Article
  17. Late adolescence mortality in mice with brain-specific deletion of the volume-regulated anion channel subunit LRRC8A.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  18. Ion Channels in Glioma Malignancy.Reviews of physiology, biochemistry and pharmacology · 2021
    Review
  19. Glial Chloride Channels in the Function of the Nervous System Across Species.Advances in experimental medicine and biology · 2021
    Article
  20. Review

20 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 2 institutions in 1 country.

Iskandar F AbdullaevOrdway Research Institute, Albany, NY 12208, USA.
Alena Rudkouskaya
Gary P Schools
Harold K Kimelberg
Alexander A Mongin
Albany Research Institute · USAlbany Medical Center Hospital · US

Funding

MECHANISMS OF INCREASED EXCITATORY AMINOACID IN ISCHEMIAR01NS035205 · NINDS · ORDWAY RESEARCH INSTITUTE, INC. · PI KIMELBERG, HAROLD K · 1996 to 2005
$2.3M
NINDS NIH HHS NS-35205NINDS NIH HHS R01 NS035205
6 · The paper itself

Abstract

Ubiquitously expressed volume-regulated anion channels (VRACs) are chloride channels which are permeable to a variety of small organic anions, including the excitatory amino acids (EAAs) glutamate and aspartate. Broad spectrum anion channel blockers strongly reduce EAA release in cerebral ischaemia and other pathological states associated with prominent astrocytic swelling. However, it is uncertain whether VRAC serves as a major pathway for EAA release from swollen cells. In the present study, we measured swelling-activated release of EAAs as D-[3H]aspartate efflux, and VRAC-mediated Cl- currents by whole-cell patch clamp in cultured rat astrocytes. We compared the pharmacological profiles of the swelling-activated EAA release pathway and Cl- currents. The expression of candidate Cl- channels was confirmed by RT-PCR. The maxi Cl- channel (p-VDAC) blocker Gd3+, the ClC-2 inhibitor Cd2+, and the MDR-1 blocker verapamil did not affect EAA release or VRAC currents. An antagonist of calcium-sensitive Cl- channels (CaCC), niflumic acid, had little effect on EAA release and only partially inhibited swelling-activated Cl- currents. The phorbol ester PDBu, which blocks ClC-3-mediated Cl- currents, had no effect on VRAC currents and up-regulated EAA release. In contrast, DCPIB, which selectively inhibits VRACs, potently suppressed both EAA release and VRAC currents. Two other relatively selective VRAC inhibitors, tamoxifen and phloretin, also blocked the VRAC currents and strongly reduced EAA release. Taken together, our data suggest that (i) astrocytic volume-dependent EAA release is largely mediated by the VRAC, and (ii) the ClC-2, ClC-3, ClC-4, ClC-5, VDAC, CaCC, MDR-1 and CFTR gene products do not contribute to EAA permeability.

Indexed as

AnimalsAnimals, NewbornAstrocytesCells, CulturedCell SizeChloride ChannelsChlorineExcitatory Amino Acid AgentsExcitatory Amino AcidsIon Channel GatingOsmotic PressureRatsRats, Sprague-DawleyWater-Electrolyte BalanceChloride ChannelsChlorineExcitatory Amino Acid AgentsExcitatory Amino Acids

Identifiers

PMID16527858
PMCPMC1780004
OpenAlexW1500192109

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.