Evidence map›Paper›PMID 24425870›Full record

ArticleThe Journal of biological chemistry2014

Differential regulation of GABAB receptor trafficking by different modes of N-methyl-D-aspartate (NMDA) receptor signaling.

Sriharsha Kantamneni, Immaculada M Gonzàlez-Gonzàlez, Jia Luo, Helena Cimarosti, Susan C Jacobs, Nadia Jaafari, Jeremy M Henley

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
  2. Action of GABAThe journal of physiological sciences : JPS · 2024
    Article
  3. Article
  4. Targeting the interaction of GABABrain pathology (Zurich, Switzerland) · 2023
    Article
  5. GABACurrent topics in behavioral neurosciences · 2022
    Review
  6. Protein phosphatase 2A regulation of GABAFrontiers in molecular neuroscience · 2022
    Article
  7. Targeting the Interaction of GABAFrontiers in pharmacology · 2022
    Article
  8. Review
  9. Sustained Baclofen-Induced Activation of GABAFrontiers in molecular neuroscience · 2021
    Article
  10. CaMolecular neurobiology · 2019
    Article
  11. Neuroadaptations of presynaptic and postsynaptic GABABritish journal of pharmacology · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. 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.

Sriharsha KantamneniSchool of Biochemistry, Medical Sciences Building, University of Bristol, Bristol BS8 1TD, United Kingdom. Electronic address: s.kantamneni@bradford.ac.uk.
Immaculada M Gonzàlez-GonzàlezSchool of Biochemistry, Medical Sciences Building, University of Bristol, Bristol BS8 1TD, United Kingdom.
Jia LuoSchool of Biochemistry, Medical Sciences Building, University of Bristol, Bristol BS8 1TD, United Kingdom.
Helena CimarostiSchool of Biochemistry, Medical Sciences Building, University of Bristol, Bristol BS8 1TD, United Kingdom.
Susan C JacobsSchool of Biochemistry, Medical Sciences Building, University of Bristol, Bristol BS8 1TD, United Kingdom.
Nadia JaafariSchool of Biochemistry, Medical Sciences Building, University of Bristol, Bristol BS8 1TD, United Kingdom.
Jeremy M HenleySchool of Biochemistry, Medical Sciences Building, University of Bristol, Bristol BS8 1TD, United Kingdom. Electronic address: J.M.Henley@bristol.ac.uk.

Funding

Biotechnology and Biological Sciences Research Council BB/F00723X/1Biotechnology and Biological Sciences Research Council BB/K014358/1Medical Research Council G0601810
6 · The paper itself

Abstract

Inhibitory GABAB receptors (GABABRs) can down-regulate most excitatory synapses in the CNS by reducing postsynaptic excitability. Functional GABABRs are heterodimers of GABAB1 and GABAB2 subunits and here we show that the trafficking and surface expression of GABABRs is differentially regulated by synaptic or pathophysiological activation of NMDA receptors (NMDARs). Activation of synaptic NMDARs using a chemLTP protocol increases GABABR recycling and surface expression. In contrast, excitotoxic global activation of synaptic and extrasynaptic NMDARs by bath application of NMDA causes the loss of surface GABABRs. Intriguingly, exposing neurons to extreme metabolic stress using oxygen/glucose deprivation (OGD) increases GABAB1 but decreases GABAB2 surface expression. The increase in surface GABAB1 involves enhanced recycling and is blocked by the NMDAR antagonist AP5. The decrease in surface GABAB2 is also blocked by AP5 and by inhibiting degradation pathways. These results indicate that NMDAR activity is critical in GABABR trafficking and function and that the individual subunits can be separately controlled to regulate neuronal responsiveness and survival.

Indexed as

AnimalsCells, CulturedCell SurvivalNeuronsProtein TransportRatsReceptors, GABA-BReceptors, N-Methyl-D-AspartateSignal TransductionStress, PhysiologicalSynapsesGabbr2 protein, ratReceptors, GABA-BReceptors, N-Methyl-D-AspartateChem-LTPGABAB ReceptorGABA ReceptorsGlutamate Receptor Ionotropic (AMPA, NMDA)G Protein-coupled Receptors (GPCR)NeurodegenerationNeurotransmitter ReceptorsOxygen-glucose Deprivation (OGD)Receptor EndocytosisReceptor Recycling

Identifiers

PMID24425870
PMCPMC3945329

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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.