Evidence map›Paper›PMID 21498812›Full record

ReviewThe Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry2011

AKAP signaling complexes in regulation of excitatory synaptic plasticity.

Jennifer L Sanderson, Mark L Dell'Acqua

Abstract readReview
In one paragraph

Review in The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

111 citing papers in PubMed, 188 citations in OpenAlex.

  1. Article
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  5. Review
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  9. Amyloid-β Causes NMDA Receptor Dysfunction and Dendritic Spine Loss through mGluR1 and AKAP150-Anchored Calcineurin Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  10. Article
  11. Protein Kinase A in neurological disorders.Journal of neurodevelopmental disorders · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. αeLife · 2023
    Article
  16. A Role for Second Messengers in Axodendritic Neuronal Polarity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Review
  17. Article
  18. Review
  19. Article
  20. Article

51 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

2 authors at 1 institution in 1 country.

Jennifer L SandersonDepartment of Pharmacology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO 80045, USA.
Mark L Dell'Acqua
University of Colorado Anschutz Medical Campus · US

Funding

Regulation of Calcium-permeable AMPA Receptors by AKAP79 Postsynaptic SignalingR01NS040701 · NINDS · UNIVERSITY OF COLORADO DENVER · PI DELL'ACQUA, MARK L · 2001 to 2023
$7.7M
BEHAVIORAL PHARMACOGENETICS OF DRUG AND ALCOHOL ABUSET32AA007464 · NIAAA · UNIVERSITY OF COLORADO DENVER · PI HOFFMAN, PAULA · 1987 to 2017
$4.8M
AKAP Regulation of Neuronal L-type Calcium Channel Signaling to the NucleusR01MH080291 · NIMH · UNIVERSITY OF COLORADO DENVER · PI DELL'ACQUA, MARK L · 2008 to 2013
$2.2M
NIAAA NIH HHS T32 AA007464NIAAA NIH HHS T32AA007464NIMH NIH HHS R01 MH080291NIMH NIH HHS R01MH080291NINDS NIH HHS R01 NS040701NINDS NIH HHS R01NS040701
6 · The paper itself

Abstract

Plasticity at excitatory glutamatergic synapses in the central nervous system is believed to be critical for neuronal circuits to process and encode information, allowing animals to perform complex behaviors such as learning and memory. In addition, alterations in synaptic plasticity are associated with human diseases, including Alzheimer disease, epilepsy, chronic pain, drug addiction, and schizophrenia. Long-term potentiation (LTP) and depression (LTD) in the hippocampal region of the brain are two forms of synaptic plasticity that increase or decrease, respectively, the strength of synaptic transmission by postsynaptic AMPA-type glutamate receptors. Both LTP and LTD are induced by activation of NMDA-type glutamate receptors but differ in the level and duration of Ca(2+) influx through the NMDA receptor and the subsequent engagement of downstream signaling by protein kinases, including PKA, PKC, and CaMKII, and phosphatases, including PP1 and calcineurin-PP2B (CaN). This review addresses the important emerging roles of the A-kinase anchoring protein family of scaffold proteins in regulating localization of PKA and other kinases and phosphatases to postsynaptic multiprotein complexes that control NMDA and AMPA receptor function during LTP and LTD.

Indexed as

A Kinase Anchor ProteinsAnimalsBrainHumansNeuronal PlasticitySignal TransductionSynaptic TransmissionA Kinase Anchor Proteins

Identifiers

PMID21498812
PMCPMC3126619
OpenAlexW2126128061

What OpenQuestion holds

Textmetadata
LicenceTDM
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.