Evidence map›Paper›PMID 22723702›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

Tonic inhibition in principal cells of the amygdala: a central role for α3 subunit-containing GABAA receptors.

Anne Marowsky, Uwe Rudolph, Jean-Marc Fritschy, Michael Arand

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

51 citing papers in PubMed, 84 citations in OpenAlex.

  1. Gene Deficiency of δ Subunit-Containing GABANeurochemical research · 2025
    Article
  2. GABA system as the cause and effect in early development.Neuroscience and biobehavioral reviews · 2024
    Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Tonic GABAergic inhibition, via GABAThe European journal of neuroscience · 2021
    Article
  9. Allosteric Modulation of GABAACS pharmacology & translational science · 2020
    Article
  10. Article
  11. Article
  12. Effects of GABAFrontiers in molecular neuroscience · 2020
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. An Emerging Circuit Pharmacology of GABATrends in pharmacological sciences · 2018
    Review
  18. Inhibition in the amygdala anxiety circuitry.Experimental & molecular medicine · 2018
    Review
  19. Article
  20. Review
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

4 authors at 2 institutions in 2 countries.

Anne MarowskyInstitute of Pharmacology and Toxicology, University of Zurich, CH-8057 Zurich, Switzerland. marowsky@pharma.uzh.ch
Uwe Rudolph
Jean-Marc Fritschy
Michael Arand
University of Zurich · CHMcLean Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

GABAergic inhibition in the amygdala is essential in regulating fear and anxiety. Although fast "phasic" inhibition arising through the activation of postsynaptic GABA(A) receptors (GABA(A)Rs) has been well described in the amygdala, much less is known about extrasynaptic GABA(A)Rs mediating persistent or tonic inhibition and regulating neuronal excitability. Here, we recorded tonic currents in the basolateral (BLA) nucleus and the lateral (LA) nucleus of the amygdala. While all BLA principal cells expressed a robust GABAergic tonic current, only 70% of LA principal cells showed a tonic current. Immunohistochemical stainings revealed that the α3 GABA(A)R subunit is expressed moderately in the LA and strongly throughout the BLA nucleus, where it is located mostly at extrasynaptic sites. In α3 subunit KO mice, tonic currents are significantly reduced in BLA principal cells yet not in LA principal cells. Moreover, the α3 GABA(A)R-selective benzodiazepine site agonist and anxiolytic compound TP003 increases tonic currents and dampens excitability markedly in wild-type BLA principal cells but fails to do so in α3KO BLA cells. Interneurons of the LA and BLA nuclei also express a tonic current, but TP003-induced potentiation is seen in only a small fraction of these cells, suggesting that primarily other GABA(A)R variants underlie tonic inhibition in this cell type. Together, these studies demonstrate that α3 GABA(A)R-mediated tonic inhibition is a central component of the inhibitory force in the amygdala and that tonically activated α3 GABA(A)Rs present an important target for anxiolytic or fear-reducing compounds.

Indexed as

AmygdalaAnimalsAnti-Anxiety AgentsBenzodiazepinesData Interpretation, StatisticalDiazepamElectrophysiological PhenomenaExcitatory Postsynaptic PotentialsFemaleGABA AgonistsGABA AntagonistsGenotypeImmunohistochemistryInterneuronsMaleMiceAnti-Anxiety AgentsBenzodiazepinesDiazepamGABA AgonistsGABA AntagonistsGabra3 protein, mouseReceptors, GABA-AReceptors, Neurotransmitter

Identifiers

PMID22723702
PMCPMC6620967
OpenAlexW1970946379

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.