Evidence map›Paper›PMID 19332484›Full record

ReviewThe Journal of physiology2009

CaMKII phosphorylation of the GABA(A) receptor: receptor subtype- and synapse-specific modulation.

Catriona M Houston, Qionger He, Trevor G Smart

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

43 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
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  7. Article
  8. Review
  9. Article
  10. GABAFrontiers in neuroscience · 2020
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Persistent CaMKII activation mediates learning-induced long-lasting enhancement of synaptic inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    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

3 authors at 1 institution in 1 country.

Catriona M HoustonDepartment of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.
Qionger He
Trevor G Smart
University College London · GB

Funding

Biotechnology and Biological Sciences Research CouncilMedical Research Council G0601529
6 · The paper itself

Abstract

As a major inhibitory neurotransmitter, GABA plays a vital role in the brain by controlling the extent of neuronal excitation. This widespread role is reflected by the ubiquitous distribution of GABA(A) receptors throughout the central nervous system. To regulate the level of neuronal inhibition requires some endogenous control over the release of GABA and/or its postsynaptic response. In this context, Ca(2+) ions are often used as primary or secondary messengers frequently resulting in the activation of protein kinases and phosphatases. One such kinase, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), can target the GABA(A) receptor to cause its phosphorylation. Evidence is now emerging, which is reviewed here, that GABA(A) receptors are indeed substrates for CaMKII and that this covalent modification alters the expression of cell surface receptors and their function. This type of regulation can also feature at inhibitory synapses leading to long-term inhibitory synaptic plasticity. Most recently, CaMKII has now been proposed to differentially phosphorylate particular isoforms of GABA(A) receptors in a synapse-specific context.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium SignalingHumansLong-Term Synaptic DepressionModels, NeurologicalPhosphorylationProtein SubunitsReceptors, GABA-ASynaptic TransmissionCalcium-Calmodulin-Dependent Protein Kinase Type 2Protein SubunitsReceptors, GABA-A

Identifiers

PMID19332484
PMCPMC2697286
OpenAlexW2129203842

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.