Evidence map›Paper›PMID 19828786›Full record

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

Extrasynaptic GABAA receptors: form, pharmacology, and function.

Delia Belelli, Neil L Harrison, Jamie Maguire, Robert L Macdonald, Matthew C Walker, David W Cope

Abstract readReview
In one paragraph

Review 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 259 papers.

0numbers the graph read from it
0cells of the map it votes in
259citing papers in PubMed
–field-weighted citation impact
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

259 citing papers in PubMed.

  1. SAGE-217, A Novel GABAClinical pharmacokinetics · 2020
    Trial
  2. Trial
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  4. Article
  5. Administration of an extrasynaptic δ-subunit GABAJournal of psychopharmacology (Oxford, England) · 2026
    Article
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  8. Review
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  15. Article
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  18. Article
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  20. Article

199 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

6 authors.

Delia BelelliDivision of Medical Sciences, Centre for Neuroscience, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, United Kingdom.
Neil L Harrison
Jamie Maguire
Robert L Macdonald
Matthew C Walker
David W Cope

Funding

Mechanisms of Propofol AnesthesiaP01GM061925 · NIGMS · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI HARRISON, NEIL L. · 2000 to 2005
$5.3M
RECOMBINANT/NATIVE GABAA RECEPTORSR01NS033300 · NINDS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MACDONALD, ROBERT LOUDEN · 1995 to 2016
$5.0M
Pathophysiology and treatment of GABRG2 nonsense epilepsy mutationsR01NS051590 · NINDS · VANDERBILT UNIVERSITY · PI MACDONALD, ROBERT LOUDEN · 2007 to 2014
$2.7M
VOLATILE ANESTHETIC INTERACTIONS WITH GABAA RECEPTORSR01GM045129 · NIGMS · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI HARRISON, NEIL L. · 1991 to 2005
$1.9M
Regulations of Neurotransmitter Action by Steroid Hormones in FemalesR01MH076994 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MODY, ISTVAN · 2007 to 2011
$1.6M
Alcohol and GABA in the ThalamusR01AA016393 · NIAAA · WEILL MEDICAL COLL OF CORNELL UNIV · PI HARRISON, NEIL L. · 2007 to 2011
$1.1M
Biotechnology and Biological Sciences Research Council BB/C509923/1Biotechnology and Biological Sciences Research Council C509923Medical Research Council G0400136Medical Research Council G0400136(70214)NIAAA NIH HHS AA16393NIAAA NIH HHS R01 AA016393NIGMS NIH HHS GM45129NIGMS NIH HHS GM61925NIGMS NIH HHS P01 GM061925NIGMS NIH HHS R01 GM045129NIMH NIH HHS MH076994NIMH NIH HHS R01 MH076994NINDS NIH HHS NS33300NINDS NIH HHS NS51590NINDS NIH HHS R01 NS033300NINDS NIH HHS R01 NS051590Wellcome Trust 071436Wellcome Trust 083163Wellcome Trust 71436Wellcome Trust WT083163MF
6 · The paper itself

Abstract

GABA is the principal inhibitory neurotransmitter in the CNS and acts via GABA(A) and GABA(B) receptors. Recently, a novel form of GABA(A) receptor-mediated inhibition, termed "tonic" inhibition, has been described. Whereas synaptic GABA(A) receptors underlie classical "phasic" GABA(A) receptor-mediated inhibition (inhibitory postsynaptic currents), tonic GABA(A) receptor-mediated inhibition results from the activation of extrasynaptic receptors by low concentrations of ambient GABA. Extrasynaptic GABA(A) receptors are composed of receptor subunits that convey biophysical properties ideally suited to the generation of persistent inhibition and are pharmacologically and functionally distinct from their synaptic counterparts. This mini-symposium review highlights ongoing work examining the properties of recombinant and native extrasynaptic GABA(A) receptors and their preferential targeting by endogenous and clinically relevant agents. In addition, it emphasizes the important role of extrasynaptic GABA(A) receptors in GABAergic inhibition throughout the CNS and identifies them as a major player in both physiological and pathophysiological processes.

Indexed as

AnimalsBiophysical PhenomenaCentral Nervous SystemFemalegamma-Aminobutyric AcidHumansMaleNeural InhibitionPregnancyPresynaptic TerminalsProtein SubunitsReceptors, GABA-ASynaptic Transmissiongamma-Aminobutyric AcidProtein SubunitsReceptors, GABA-A

Identifiers

PMID19828786
PMCPMC2784229

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.