Evidence map›Paper›PMID 20725525›Full record

ArticleFrontiers in cellular neuroscience2010

Temporal coding at the immature depolarizing GABAergic synapse.

Guzel Valeeva, Azat Abdullin, Roman Tyzio, Andrei Skorinkin, Evgeny Nikolski, Yehezkiel Ben-Ari, Rustem Khazipov

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.7field-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

36 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Delaying the GABA Shift Indirectly Affects Membrane Properties in the Developing Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. When Are Depolarizing GABAergic Responses Excitatory?Frontiers in molecular neuroscience · 2021
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. GABAergic Synchronization in Epilepsy.Cold Spring Harbor perspectives in medicine · 2016
    Review
  14. Article
  15. Article
  16. Depolarizing GABA and developmental epilepsies.CNS neuroscience & therapeutics · 2015
    Review
  17. Article
  18. Article
  19. Glycine transporter-1 controls nonsynaptic inhibitory actions of glycine receptors in the neonatal rat hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    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

7 authors at 1 institution in 2 countries.

Guzel ValeevaInstitut de Neurobiologie de la Méditerranée-Institut National de la Santé et de la Recherche Médicale U901, Universite Mediterranean Aix-Marseille II Marseille, France.
Azat Abdullin
Roman Tyzio
Andrei Skorinkin
Evgeny Nikolski
Yehezkiel Ben-Ari
Rustem Khazipov
Kazan Institute of Biochemistry and Biophysics · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the developing hippocampus, GABA exerts depolarizing and excitatory actions and contributes to the generation of neuronal network driven giant depolarizing potentials (GDPs). Here, we studied spike time coding at immature GABAergic synapses and its impact on synchronization of the neuronal network during GDPs in the neonatal (postnatal days P2-6) rat hippocampal slices. Using extracellular recordings, we found that the delays of action potentials (APs) evoked by synaptic activation of GABA(A) receptors are long (mean, 65 ms) and variable (within a time window of 10-200 ms). During patch-clamp recordings, depolarizing GABAergic responses were mainly subthreshold and their amplification by persistent sodium conductance was required to trigger APs. AP delays at GABAergic synapses shortened and their variability reduced with an increase in intracellular chloride concentration during whole-cell recordings. Negative shift of the GABA reversal potential (E(GABA)) with low concentrations of bumetanide, or potentiation of GABA(A) receptors with diazepam reduced GDPs amplitude, desynchronized neuronal firing during GDPs and slowed down GDPs propagation. Partial blockade of GABA(A) receptors with bicuculline increased neuronal synchronization and accelerated GDPs propagation. We propose that spike timing at depolarizing GABA synapses is determined by intracellular chloride concentration. At physiological levels of intracellular chloride GABAergic depolarization does not reach the action potential threshold and amplification of GABAergic responses by non-inactivating sodium conductance is required for postsynaptic AP initiation. Slow and variable excitation at GABAergic synapse determines the level of neuronal synchrony and the rate of GDPs propagation in the developing hippocampus.

Indexed as

developmentgamma aminobutyric acidhippocampusneonatal

Identifiers

PMID20725525
PMCPMC2914581
OpenAlexW2169879728

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.