Evidence map›Paper›PMID 24167475›Full record

ReviewFrontiers in neural circuits2013

Pathophysiological power of improper tonic GABA(A) conductances in mature and immature models.

Kiyoshi Egawa, Atsuo Fukuda

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neural circuits, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 53 citations in OpenAlex.

  1. Trial
  2. GABACellular and molecular neurobiology · 2026
    Review
  3. Review
  4. Article
  5. Physiological roles of chloride ions in bodily and cellular functions.The journal of physiological sciences : JPS · 2023
    Review
  6. Maternal taurine as a modulator of ClFrontiers in cellular neuroscience · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Electrophysiology of ionotropic GABA receptors.Cellular and molecular life sciences : CMLS · 2021
    Review
  12. When Are Depolarizing GABAergic Responses Excitatory?Frontiers in molecular neuroscience · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. GABA-mediated tonic inhibition differentially modulates gain in functional subtypes of cortical interneurons.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  17. Article
  18. Article
  19. Article
  20. Comparison of αβδ and αβγ GABAPharmacological research · 2018
    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

2 authors at 2 institutions in 2 countries.

Kiyoshi EgawaDepartment of Neurology, Massachusetts General Hospital Charlestown, MA, USA ; Department of Pediatrics, Hokkaido University Graduate School of Medicine Sapporo, Japan.
Atsuo Fukuda
Hamamatsu University School of Medicine · JPHokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-affinity extrasynaptic gamma-aminobutyric acid A (GABA(A)) receptors are tonically activated by low and consistent levels of ambient GABA, mediating chronic inhibition against neuronal excitability (tonic inhibition) and the modulation of neural development. Synaptic (phasic) inhibition is spatially and temporally precise compared with tonic inhibition, which provides blunt yet strong integral inhibitory force by shunting electrical signaling. Although effects of acute modification of tonic inhibition are known, its pathophysiological significance remains unclear because homeostatic regulation of neuronal excitability can compensate for long-term deficit of extrasynaptic GABA(A) receptor activation. Nevertheless, tonic inhibition is of great interest for its pathophysiological involvement in central nervous system (CNS) diseases and thus as a therapeutic target. Together with the development of experimental models for various pathological states, recent evidence demonstrates such pathological involvements of tonic inhibition in neuronal dysfunction. This review focuses on the recent progress of tonic activation of GABA(A) conductance on the development and pathology of the CNS. Findings indicate that neuronal function in various brain regions are exacerbated with a gain or loss of function of tonic inhibition by GABA spillover. Disturbance of tonic GABA(A) conductance mediated by non-synaptic ambient GABA may result in brain mal-development. Therefore, various pathological states (epilepsy, motor dysfunctions, psychiatric disorders, and neurodevelopmental disorders) may be partly attributable to abnormal tonic GABA(A) conductances. Thus, the tone of tonic conductance and level of ambient GABA may be precisely tuned to maintain the regular function and development of the CNS. Therefore, receptor expression and factors for regulating the ambient GABA concentration are highlighted to gain a deeper understanding of pathology and therapeutic strategy for CNS diseases.

Indexed as

Animalsgamma-Aminobutyric AcidHippocampusNeural ConductionNeural InhibitionNeuronsReceptors, GABA-Agamma-Aminobutyric AcidReceptors, GABA-AambientextrasynapticGABAGABAA receptorGATneurological diseasetonic inhibitiontransporter

Identifiers

PMID24167475
PMCPMC3807051
OpenAlexW1965934941

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.