Evidence map›Paper›PMID 12843287›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

NMDA and beta1-adrenergic receptors differentially signal phosphorylation of glutamate receptor type 1 in area CA1 of hippocampus.

Amanda M Vanhoose, Danny G Winder

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
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, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Norepinephrine Induces PTSD-Like Memory ImpairmentsFrontiers in behavioral neuroscience · 2019
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Stress induces pain transition by potentiation of AMPA receptor phosphorylation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  9. Article
  10. The developmental stages of synaptic plasticity.The Journal of physiology · 2014
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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  19. Review
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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

2 authors at 1 institution in 1 country.

Amanda M VanhooseDepartment of Molecular Physiology and Biophysics, Center for Molecular Neuroscience, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0615, USA.
Danny G Winder
John F. Kennedy Center for the Performing Arts · US

Funding

TRAINING PROGRAM IN CELLULAR, BIOCHEMICAL, &MOLECULAR ST32GM008554 · NIGMS · VANDERBILT UNIVERSITY · PI PATTON, JAMES G. · 1995 to 2020
$7.4M
Regulation of LTP by Gi Linked ReceptorsR01DA013699 · NIDA · VANDERBILT UNIVERSITY · PI WINDER, DANNY G · 2001 to 2004
$1.1M
NIDA NIH HHS DA13699NIDA NIH HHS R01 DA013699NIGMS NIH HHS T32 GM008554NIGMS NIH HHS T32 GM08554
6 · The paper itself

Abstract

Glutamatergic synaptic transmission is mediated primarily through the AMPA-type glutamate receptor (AMPAR); the regulation of this receptor underlies many forms of synaptic plasticity. In particular, phosphorylation of GluR1, an AMPAR subunit, by PKA at serine 845 (S845) increases peak open channel probability and is permissive for both the synaptic expression of the receptor and NMDA-receptor (NMDAR)-dependent long-term potentiation (LTP). Robust NMDAR activation activates PKA as well as other signaling enzymes; however, we find that maximal NMDAR activation dephosphorylates GluR1 at the PKA site S845. Coincident inhibition of phosphatases blocks NMDAR-induced dephosphorylation of S845, but surprisingly does not promote PKA phosphorylation at this site. However, we find that phosphorylation of S845 is increased by the activation of a Gs-coupled receptor, the beta1-adrenergic receptor. Interestingly, this divergent signaling occurs despite a more robust coupling of the NMDAR to cAMP generation. In addition, NMDAR activation plays a dominant role in S845 regulation, because activation of beta1AR after NMDAR activation has no detectable effect on S845 phosphorylation. These data (1) demonstrate highly specific coupling between these receptors and this substrate, (2) provide an example of a substrate critical in NMDAR-dependent LTP that is incompletely regulated by the NMDAR, and (3) highlight the importance of identifying the physiological signals that regulate these critical synaptic substrates.

Indexed as

Adrenergic AntagonistsAdrenergic beta-1 Receptor AntagonistsAdrenergic beta-AgonistsAmino Acids, CyclicAnimalsCyclic AMP-Dependent Protein KinasesDose-Response Relationship, DrugExcitatory Postsynaptic PotentialsHippocampusIn Vitro TechniquesLong-Term PotentiationMaleMiceMice, Inbred C57BLNeuronal PlasticityN-MethylaspartateAdrenergic AntagonistsAdrenergic beta-1 Receptor AntagonistsAdrenergic beta-AgonistsAmino Acids, CyclicCyclic AMP-Dependent Protein KinasesN-MethylaspartateReceptors, Adrenergic, beta-1Receptors, AMPAReceptors, N-Methyl-D-Aspartate

Identifiers

PMID12843287
PMCPMC6741229
OpenAlexW1596299456

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.