Evidence map›Paper›PMID 24102973›Full record

ArticleThe European journal of neuroscience2013

Protein kinase C regulates tonic GABA(A) receptor-mediated inhibition in the hippocampus and thalamus.

Damian P Bright, Trevor G Smart

Open access · hybridAbstract read
In one paragraph

Article in The European journal of neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. Tonic GABAScientific reports · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Silencing of spontaneous activity at α4β1/3δ GABABritish journal of pharmacology · 2020
    Article
  8. The Functional Role of Spontaneously Opening GABAFrontiers in molecular neuroscience · 2019
    Article
  9. Feature Article: Selective modulation of tonically active GABAExperimental biology and medicine (Maywood, N.J.) · 2018
    Article
  10. Spontaneously opening GABACell death & disease · 2018
    Article
  11. Single Ethanol Withdrawal Regulates Extrasynaptic δ-GABAFrontiers in molecular neuroscience · 2018
    Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Basal ganglia-thalamus and the "crowning enigma".Frontiers in neural circuits · 2015
    Review
  20. Regulation of GABAARs by phosphorylation.Advances in pharmacology (San Diego, Calif.) · 2015
    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 1 institution in 1 country.

Damian P BrightDepartment of Neuroscience, Physiology & Pharmacology, University College London, Gower Street, London, WC1E 6BT, UK.
Trevor G Smart
University College London · GB

Funding

Medical Research Council MR/K005537/1
6 · The paper itself

Abstract

Tonic inhibition mediated by extrasynaptic GABA(A) receptors (GABA(A) Rs) is an important regulator of neuronal excitability. Phosphorylation by protein kinase C (PKC) provides a key mode of regulation for synaptic GABA(A) Rs underlying phasic inhibition; however, less attention has been focused on the plasticity of tonic inhibition and whether this can also be modulated by receptor phosphorylation. To address this issue, we used whole-cell patch clamp recording in acute murine brain slices at both room and physiological temperatures to examine the effects of PKC-mediated phosphorylation on tonic inhibition. Recordings from dentate gyrus granule cells in the hippocampus and dorsal lateral geniculate relay neurons in the thalamus demonstrated that PKC activation caused downregulation of tonic GABA(A) R-mediated inhibition. Conversely, inhibition of PKC resulted in an increase in tonic GABA(A) R activity. These findings were corroborated by experiments on human embryonic kidney 293 cells expressing recombinant α4β2δ GABA(A) Rs, which represent a key extrasynaptic GABA(A) R isoform in the hippocampus and thalamus. Using bath application of low GABA concentrations to mimic activation by ambient neurotransmitter, we demonstrated a similar inhibition of receptor function following PKC activation at physiological temperature. Live cell imaging revealed that this was correlated with a loss of cell surface GABA(A) Rs. The inhibitory effects of PKC activation on α4β2δ GABA(A) R activity appeared to be mediated by direct phosphorylation at a previously identified site on the β2 subunit, serine 410. These results indicate that PKC-mediated phosphorylation can be an important physiological regulator of tonic GABA(A) R-mediated inhibition.

Indexed as

AnimalsEnzyme Activationgamma-Aminobutyric AcidHEK293 CellsHippocampusHumansMiceNeural InhibitionOrgan Culture TechniquesProtein Kinase CReceptors, GABA-AThalamusgamma-Aminobutyric AcidProtein Kinase CReceptors, GABA-AGABAA receptormousePKCtonic inhibition

Identifiers

PMID24102973
PMCPMC4165308
OpenAlexW2089091885

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.