Evidence map›Paper›PMID 16624942›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

Ambient GABA constrains the strength of GABAergic synapses at Cajal-Retzius cells in the developing visual cortex.

Knut Kirmse, Sergei Kirischuk

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

39 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Tonic activation of GABAFrontiers in synaptic neuroscience · 2023
    Article
  6. GABA Release from Astrocytes in Health and Disease.International journal of molecular sciences · 2022
    Review
  7. Keeping the Balance: GABABrain sciences · 2022
    Review
  8. Review
  9. Osmotic Demyelination: From an Oligodendrocyte to an Astrocyte Perspective.International journal of molecular sciences · 2019
    Review
  10. Review
  11. Activating Transcription Factor 4 (ATF4) Regulates Neuronal Activity by Controlling GABAThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Anion transport and GABA signaling.Frontiers in cellular neuroscience · 2013
    Review
  18. Article
  19. Rapid, activity-independent turnover of vesicular transmitter content at a mixed glycine/GABA synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  20. 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.

Knut KirmseSensory and Developmental Physiology Group, Institute of Neurophysiology, Johannes-Mueller-Center of Physiology, Charité-University Medicine Berlin, 10117 Berlin, Germany.
Sergei Kirischuk
Charité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

At early stages of brain development, GABA plays a dual role. It fulfills important trophic functions and provides a major excitatory drive for the immature neuronal network. Here, we investigated whether GABA itself can limit the strength of excitatory GABAergic synapses on Cajal-Retzius (CR) cells in sagittal slices from the mouse visual cortex. (2S)-3-[[(1S)-1-(3,4-dichlorophenyl)ethyl]amino-2-hydroxypropyl](phenylmethyl)phosphinic acid (CGP55845), a specific GABAB receptor (GABABR) blocker, increased the frequency of spontaneous Ca2+ transients and spontaneous and miniature IPSCs (mIPSCs) but did not affect mIPSC amplitudes or kinetics. CGP55845 significantly increased evoked IPSC (eIPSC) amplitudes and decreased the paired-pulse ratio (PPR). Baclofen, a specific GABABR agonist, produced opposite effects. The size of the readily releasable pool was not affected by these GABABR modulators. The same CGP55845 actions were observed at physiological temperatures, but they were abolished after glutamate decarboxylase block with 3-mercaptopropionic acid (3-MP). These results indicate that presynaptic GABABRs dynamically regulate GABA release probability. SNAP-5114, a specific GABA transporter-2/3 (GAT-2/3) blocker, enhanced mIPSC frequencies, decreased PPR, and increased eIPSC amplitudes without changing eIPSC kinetics. These effects were blocked by CGP55845 and 3-MP. NO-711, a specific GAT-1 blocker, prolonged eIPSC decay and decreased eIPSC/mIPSC amplitudes. These NO-711-mediated effects were not sensitive to CGP55845 and 3-MP. We conclude that the strength of GABAergic inputs to CR cells is constrained by GABABRs that are persistently activated by ambient GABA. The latter is also provided by GAT-2/3 operating in the reversed mode. Presynaptic GAT-1 functions in the uptake mode and possibly provides GABA for presynaptic vesicle filling.

Indexed as

AnimalsAnimals, NewbornGABA AntagonistsGABA-B Receptor Antagonistsgamma-Aminobutyric AcidMiceMice, Inbred C57BLReceptors, GABA-BSynapsesVisual CortexGABA AntagonistsGABA-B Receptor Antagonistsgamma-Aminobutyric AcidReceptors, GABA-B

Identifiers

PMID16624942
PMCPMC6674013
OpenAlexW2030230530

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.