Evidence map›Paper›PMID 21106838›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

GABA depolarizes immature neocortical neurons in the presence of the ketone body ß-hydroxybutyrate.

Knut Kirmse, Otto W Witte, Knut Holthoff

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Anion transport and GABA signaling.Frontiers in cellular neuroscience · 2013
    Review
  11. Ketone bodies in epilepsy.Journal of neurochemistry · 2012
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Chronic hyperosmotic stress converts GABAergic inhibition into excitation in vasopressin and oxytocin neurons in the rat.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  17. Article
  18. Review
  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

Knut KirmseExperimentelle Neurologie, Hans-Berger-Klinik für Neurologie, Universitätsklinikum Jena, 07747 Jena, Germany. knut.kirmse@med.uni-jena.de
Otto W Witte
Knut Holthoff
Jena University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A large body of evidence suggests that the neurotransmitter GABA undergoes a developmental switch from being predominantly depolarizing-excitatory to predominantly hyperpolarizing-inhibitory. Recently published data, however, point to the possibility that the presumed depolarizing mode of GABA action during early development might represent an artifact due to an insufficient energy supply of the in vitro preparations used. Specifically, addition of the ketone body dl-β-hydroxybutyrate (βHB) to the extracellular medium was shown to prevent GABA from exerting excitatory effects. Applying a complementary set of minimally invasive optical and electrophysiological techniques in brain slices from neonatal mice, we investigated the effects of βHB on GABA actions in immature cells of the upper cortical plate. Fluorescence imaging revealed that GABA-mediated somatic [Ca(2+)] transients, that required activation of GABA(A) receptors and voltage-gated Ca(2+) channels, remained unaffected by βHB. Cell-attached current-clamp recordings showed that, in the presence of βHB, GABA still induced a membrane potential depolarization. To estimate membrane potential changes quantitatively, we used cell-attached recordings of voltage-gated potassium currents and demonstrated that the GABA-mediated depolarization was independent of supplementation of the extracellular solution with βHB. We conclude that, in vitro, GABA depolarizes immature cells of the upper cortical plate in the presence of the ketone body βHB. Our data thereby support the general concept of an excitatory-to-inhibitory switch of GABA action during early development.

Indexed as

3-Hydroxybutyric AcidAnimalsAnimals, NewbornDrug Synergismgamma-Aminobutyric AcidKetone BodiesMembrane PotentialsMiceMice, Inbred C57BLNeocortexNeurons3-Hydroxybutyric Acidgamma-Aminobutyric AcidKetone Bodies

Identifiers

PMID21106838
PMCPMC6633760
OpenAlexW2157025435

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.