Evidence map›Paper›PMID 21209187›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Depolarizing actions of GABA in immature neurons depend neither on ketone bodies nor on pyruvate.

Roman Tyzio, Camille Allene, Romain Nardou, Michel A Picardo, Sumii Yamamoto, Sudhir Sivakumaran, Maddalena D Caiati, Sylvain Rheims, Marat Minlebaev, Mathieu Milh and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.9field-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

26 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Ketone bodies in epilepsy.Journal of neurochemistry · 2012
    Review
  10. Traumatic alterations in GABA signaling disrupt hippocampal network activity in the developing brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. 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
  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

19 authors at 8 institutions in 3 countries.

Roman TyzioInserm, Unité 901/Institut de Neurobiologie de Méditerranée, 13273 Marseille, France.
Camille Allene
Romain Nardou
Michel A Picardo
Sumii Yamamoto
Sudhir Sivakumaran
Maddalena D Caiati
Sylvain Rheims
Marat Minlebaev
Mathieu Milh
Pascal Ferré
Rustem Khazipov
Jean-Louis Romette
Jean Lorquin
Rosa Cossart
Ilgam Khalilov
Astrid Nehlig
Enrico Cherubini
Yehezkel Ben-Ari
Institut de Neurobiologie de la Méditerranée · FRInserm · FRAix-Marseille Université · FRTecnologie Avanzate (Italy) · ITCentre d’Immunologie de Marseille-Luminy · FRInstitut de Biosciences et Biotechnologies · FRScuola Internazionale Superiore di Studi Avanzati · ITUniversité de Strasbourg · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

GABA depolarizes immature neurons because of a high [Cl(-)](i) and orchestrates giant depolarizing potential (GDP) generation. Zilberter and coworkers (Rheims et al., 2009; Holmgren et al., 2010) showed recently that the ketone body metabolite DL-3-hydroxybutyrate (DL-BHB) (4 mM), lactate (4 mM), or pyruvate (5 mM) shifted GABA actions to hyperpolarizing, suggesting that the depolarizing effects of GABA are attributable to inadequate energy supply when glucose is the sole energy source. We now report that, in rat pups (postnatal days 4-7), plasma D-BHB, lactate, and pyruvate levels are 0.9, 1.5, and 0.12 mM, respectively. Then, we show that DL-BHB (4 mM) and pyruvate (200 μM) do not affect (i) the driving force for GABA(A) receptor-mediated currents (DF(GABA)) in cell-attached single-channel recordings, (2) the resting membrane potential and reversal potential of synaptic GABA(A) receptor-mediated responses in perforated patch recordings, (3) the action potentials triggered by focal GABA applications, or (4) the GDPs determined with electrophysiological recordings and dynamic two-photon calcium imaging. Only very high nonphysiological concentrations of pyruvate (5 mM) reduced DF(GABA) and blocked GDPs. Therefore, DL-BHB does not alter GABA signals even at the high concentrations used by Zilberter and colleagues, whereas pyruvate requires exceedingly high nonphysiological concentrations to exert an effect. There is no need to alter conventional glucose enriched artificial CSF to investigate GABA signals in the developing brain.

Indexed as

3-Hydroxybutyric AcidAction PotentialsAnimalsAnimals, NewbornBicucullineBrainBumetanideCalciumDose-Response Relationship, DrugExcitatory Amino Acid AntagonistsFemaleGABA-A Receptor Antagonistsgamma-Aminobutyric AcidIn Vitro TechniquesKetone BodiesLactic Acid3-Hydroxybutyric AcidBicucullineBumetanideCalciumExcitatory Amino Acid AntagonistsGABA-A Receptor Antagonistsgamma-Aminobutyric AcidKetone BodiesLactic AcidPyruvic AcidSodium Potassium Chloride Symporter Inhibitors

Identifiers

PMID21209187
PMCPMC6622726
OpenAlexW2090706409

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.