Evidence map›Paper›PMID 25852540›Full record

ArticleFrontiers in synaptic neuroscience2015

Compartmental distribution of GABAB receptor-mediated currents along the somatodendritic axis of hippocampal principal cells.

Claudius E Degro, Akos Kulik, Sam A Booker, Imre Vida

Open access · goldAbstract read
In one paragraph

Article in Frontiers in synaptic neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. GABAeNeuro · 2026
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  3. Phylogenetic divergence of GABANature communications · 2025
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  4. G protein-gated inwardly rectifying KHistology and histopathology · 2025
    Review
  5. Article
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  7. Article
  8. Article
  9. Review
  10. Nanoscale alterations in GABAAlzheimer's research & therapy · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Keeping the Balance: GABABrain sciences · 2022
    Review
  15. Article
  16. Article
  17. Reduction in the neuronal surface of post and presynaptic GABABrain pathology (Zurich, Switzerland) · 2020
    Article
  18. Density of GABAInternational journal of molecular sciences · 2020
    Article
  19. Presynaptic GABAeLife · 2020
    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

4 authors at 2 institutions in 1 country.

Claudius E DegroInstitute for Integrative Neuroanatomy, Neurocure Cluster of Excellence, Charité Universitätsmedizin Berlin Germany.
Akos KulikInstitute for Physiology II, Bioss Centre for Biological Signalling Studies, University of Freiburg Freiburg Germany.
Sam A BookerInstitute for Integrative Neuroanatomy, Neurocure Cluster of Excellence, Charité Universitätsmedizin Berlin Germany.
Imre VidaInstitute for Integrative Neuroanatomy, Neurocure Cluster of Excellence, Charité Universitätsmedizin Berlin Germany.
Charité - Universitätsmedizin Berlin · DEUniversity of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activity of cortical principal cells is controlled by the GABAergic system providing inhibition in a compartmentalized manner along their somatodendritic axis. While GABAAR-mediated inhibitory synaptic transmission has been extensively characterized in hippocampal principal cells, little is known about the distribution of postsynaptic effects of GABABRs. In the present study, we have investigated the functional localization of GABABRs and their effector inwardly rectifying potassium (Kir3) channels by combining electrophysiological recordings in acute rat hippocampal slices, high-resolution immunoelectron microscopic analysis and single cell simulations. Pharmacologically isolated slow inhibitory postsynaptic currents were elicited in the three major hippocampal principal cell types by endogenous GABA released by electrical stimulation, photolysis of caged-GABA, as well as the canonical agonist baclofen, with the highest amplitudes observed in the CA3. Spatially restricted currents were assessed along the axis of principal cells by uncaging GABA in the different hippocampal layers. GABABR-mediated currents were present along the entire somatodendritic axis of principal cells, but non-uniformly distributed: largest currents and the highest conductance densities determined in the simulations were consistently found on the distal apical dendrites. Finally, immunocytochemical localization of GABABRs and Kir3 channels showed that distributions overlap but their densities diverge, particularly on the basal dendrites of pyramidal cells. GABABRs current amplitudes and the conductance densities correlated better with Kir3 density, suggesting a bottlenecking effect defined by the effector channel. These data demonstrate a compartmentalized distribution of the GABABR-Kir3 signaling cascade and suggest differential control of synaptic transmission, dendritic integration and synaptic plasticity at afferent pathways onto hippocampal principal cells.

Indexed as

dendritesGABAB-receptorhippocampusinhibitionKir3-channelprincipal cells

Identifiers

PMID25852540
PMCPMC4369648
OpenAlexW2045699451

What OpenQuestion holds

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Registered trials

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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.