Evidence map›Paper›PMID 18596171›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008

GABA(B) receptor modulation of feedforward inhibition through hippocampal neurogliaform cells.

Christopher J Price, Ricardo Scott, Dmitri A Rusakov, Marco Capogna

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
2.9field-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

62 citing papers in PubMed, 103 citations in OpenAlex.

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  14. Review
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  16. GABAFrontiers in cellular neuroscience · 2021
    Article
  17. GABAFrontiers in integrative neuroscience · 2021
    Article
  18. Review
  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Christopher J PriceMedical Research Council Anatomical Neuropharmacology Unit, Oxford OX1 3TH, United Kingdom.
Ricardo Scott
Dmitri A Rusakov
Marco Capogna
Medical Research Council · GBUniversity College London · GB

Funding

Medical Research Council G0400627Medical Research Council G0400627(71256)Medical Research Council G0400627(76527)Medical Research Council G0600368Medical Research Council G0600368(77987)Medical Research Council MC_U138197106Wellcome Trust 071179Wellcome Trust 084311
6 · The paper itself

Abstract

Feedforward inhibition of neurons is a fundamental component of information flow control in the brain. We studied the roles played by neurogliaform cells (NGFCs) of stratum lacunosum moleculare of the hippocampus in providing feedforward inhibition to CA1 pyramidal cells. We recorded from synaptically coupled pairs of anatomically identified NGFCs and CA1 pyramidal cells and found that, strikingly, a single presynaptic action potential evoked a biphasic unitary IPSC (uIPSC), consisting of two distinct components mediated by GABA(A) and GABA(B) receptors. A GABA(B) receptor-mediated unitary response has not previously been observed in hippocampal excitatory neurons. The decay of the GABA(A) receptor-mediated response was slow (time constant = 50 ms), and was tightly regulated by presynaptic GABA(B) receptors. Surprisingly, the GABA(B) receptor ligands baclofen and (2S)-3-{[(1S)-1-(3,4-dichlorophenyl)ethyl]amino-2-hydroxypropyl}(phenylmethyl)phosphinic acid (CGP55845), while affecting the NGFC-mediated uIPSCs, had no effect on action potential-evoked presynaptic Ca2+ signals monitored in individual axonal boutons of NGFCs with two-photon microscopy. In contrast, baclofen clearly depressed presynaptic Ca2+ transients in non-NGF interneurons. Changes in extracellular Ca2+ concentration that mimicked the effects of baclofen or CGP55845 on uIPSCs significantly altered presynaptic Ca2+ transients. Electrophysiological data suggest that GABA(B) receptors expressed by NGFCs contribute to the dynamic control of the excitatory input to CA1 pyramidal neurons from the temporoammonic path. The NGFC-CA1 pyramidal cell connection therefore provides a unique and subtle mechanism to shape the integration time domain for signals arriving via a major excitatory input to CA1 pyramidal cells.

Indexed as

Action PotentialsAnimalsBaclofenCalciumCalcium SignalingGABA AgonistsGABA Antagonistsgamma-Aminobutyric AcidHippocampusInhibitory Postsynaptic PotentialsInterneuronsNeural InhibitionNeural PathwaysNeurogliaOrgan Culture TechniquesPhosphinic AcidsBaclofenCalciumCGP 55845AGABA AgonistsGABA Antagonistsgamma-Aminobutyric AcidPhosphinic AcidsPropanolaminesReceptors, GABA-AReceptors, GABA-B

Identifiers

PMID18596171
PMCPMC2685170
OpenAlexW2036270719

What OpenQuestion holds

Textmetadata
LicenceTDM
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.