Evidence map›Paper›PMID 15240800›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Redistribution of GABAB(1) protein and atypical GABAB responses in GABAB(2)-deficient mice.

Martin Gassmann, Hamdy Shaban, Réjan Vigot, Gilles Sansig, Corinne Haller, Samuel Barbieri, Yann Humeau, Valérie Schuler, Matthias Müller, Bernd Kinzel and 16 more

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
–field-weighted citation impact
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

92 citing papers in PubMed.

  1. Article
  2. Article
  3. Central Dysmyelination in SSADH-Deficient Humans and Mice.Annals of clinical and translational neurology · 2025
    Observational
  4. Review
  5. Article
  6. Article
  7. GABAJournal of neurochemistry · 2025
    Article
  8. Genetic implication of GABAFrontiers in pharmacology · 2025
    Review
  9. Article
  10. Novel-Type GABAACS medicinal chemistry letters · 2024
    Article
  11. Article
  12. Sigma-1 receptor and seizures.Pharmacological research · 2023
    Review
  13. Article
  14. Keeping the Balance: GABABrain sciences · 2022
    Review
  15. GABACurrent topics in behavioral neurosciences · 2022
    Review
  16. Mechanisms and Regulation of Neuronal GABACurrent topics in behavioral neurosciences · 2022
    Review
  17. Review
  18. GABACurrent topics in behavioral neurosciences · 2022
    Review
  19. GABACurrent topics in behavioral neurosciences · 2022
    Article
  20. Review

32 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

26 authors.

Martin GassmannPharmazentrum, Department of Clinical-Biological Sciences, University of Basel, CH-4056 Basel, Switzerland.
Hamdy Shaban
Réjan Vigot
Gilles Sansig
Corinne Haller
Samuel Barbieri
Yann Humeau
Valérie Schuler
Matthias Müller
Bernd Kinzel
Klaus Klebs
Markus Schmutz
Wolfgang Froestl
Jakob Heid
Peter H Kelly
Clive Gentry
Anne-Lise Jaton
Herman Van der Putten
Cédric Mombereau
Lucas Lecourtier
Johannes Mosbacher
John F Cryan
Jean-Marc Fritschy
Andreas Lüthi
Klemens Kaupmann
Bernhard Bettler

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

GABAB receptors mediate slow synaptic inhibition in the nervous system. In transfected cells, functional GABAB receptors are usually only observed after coexpression of GABAB(1) and GABAB(2) subunits, which established the concept of heteromerization for G-protein-coupled receptors. In the heteromeric receptor, GABAB(1) is responsible for binding of GABA, whereas GABAB(2) is necessary for surface trafficking and G-protein coupling. Consistent with these in vitro observations, the GABAB(1) subunit is also essential for all GABAB signaling in vivo. Mice lacking the GABAB(1) subunit do not exhibit detectable electrophysiological, biochemical, or behavioral responses to GABAB agonists. However, GABAB(1) exhibits a broader cellular expression pattern than GABAB(2), suggesting that GABAB(1) could be functional in the absence of GABAB(2). We now generated GABAB(2)-deficient mice to analyze whether GABAB(1) has the potential to signal without GABAB(2) in neurons. We show that GABAB(2)-/- mice suffer from spontaneous seizures, hyperalgesia, hyperlocomotor activity, and severe memory impairment, analogous to GABAB(1)-/- mice. This clearly demonstrates that the lack of heteromeric GABAB(1,2) receptors underlies these phenotypes. To our surprise and in contrast to GABAB(1)-/- mice, we still detect atypical electrophysiological GABAB responses in hippocampal slices of GABAB(2)-/- mice. Furthermore, in the absence of GABAB(2), the GABAB(1) protein relocates from distal neuronal sites to the soma and proximal dendrites. Our data suggest that association of GABAB(2) with GABAB(1) is essential for receptor localization in distal processes but is not absolutely necessary for signaling. It is therefore possible that functional GABAB receptors exist in neurons that naturally lack GABAB(2) subunits.

Indexed as

AnimalsBrainBrain ChemistryDimerizationElectroencephalographyGABA AgonistsHippocampusHyperalgesiaHyperkinesisMemory DisordersMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutNeuronsPain MeasurementGABA AgonistsPotassium ChannelsProtein SubunitsReceptors, GABA-B

Identifiers

PMID15240800
PMCPMC6729668

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.