Evidence map›Paper›PMID 21525283›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Protein kinase M maintains long-term sensitization and long-term facilitation in aplysia.

Diancai Cai, Kaycey Pearce, Shanping Chen, David L Glanzman

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing 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

56 citing papers in PubMed.

  1. Article
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  7. Review
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  10. Review
  11. Excitatory postsynaptic calcium transients atLearning & memory (Cold Spring Harbor, N.Y.) · 2021
    Article
  12. Article
  13. Article
  14. Isoform Specificity of PKMs during Long-Term Facilitation inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  15. Review
  16. Review
  17. Article
  18. PKMζ Inhibition Disrupts Reconsolidation and Erases Object Recognition Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  19. Review
  20. Autocrine signaling by anProceedings of the National Academy of Sciences of the United States of America · 2018
    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

4 authors.

Diancai CaiDepartment of Integrative Biology and Physiology, University of California, Los Angeles, College, Los Angeles, California 90095-1606, USA.
Kaycey Pearce
Shanping Chen
David L Glanzman

Funding

Hebbian Long-Term Potentiation and Learning in AplysiaR37NS029563 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GLANZMAN, DAVID L · 2005 to 2011
$2.9M
NINDS NIH HHS R37 NS029563
6 · The paper itself

Abstract

How the brain maintains long-term memories is one of the major outstanding questions in modern neuroscience. Evidence from mammalian studies indicates that activity of a protein kinase C (PKC) isoform, protein kinase Mζ (PKMζ), plays a critical role in the maintenance of long-term memory. But the range of memories whose persistence depends on PKMζ, and the mechanisms that underlie the effect of PKMζ on long-term memory, remain obscure. Recently, a PKM isoform, known as PKM Apl III, was cloned from the nervous system of Aplysia. Here, we tested whether PKM Apl III plays a critical role in long-term memory maintenance in Aplysia. Intrahemocoel injections of the pseudosubstrate inhibitory peptide ZIP (ζ inhibitory peptide) or the PKC inhibitor chelerythrine erased the memory for long-term sensitization (LTS) of the siphon-withdrawal reflex (SWR) as late as 7 d after training. In addition, both PKM inhibitors disrupted the maintenance of long-term (≥ 24 h) facilitation (LTF) of the sensorimotor synapse, a form of synaptic plasticity previously shown to mediate LTS of the SWR. Together with previous results (Bougie et al., 2009), our results support the idea that long-term memory in Aplysia is maintained via a positive-feedback loop involving PKM Apl III-dependent protein phosphorylation. The present data extend the known role of PKM in memory maintenance to a simple and well studied type of long-term learning. Furthermore, the demonstration that PKM activity underlies the persistence of LTF of the Aplysia sensorimotor synapse, a form of synaptic plasticity amenable to rigorous cellular and molecular analyses, should facilitate efforts to understand how PKM activity maintains memory.

Indexed as

Analysis of VarianceAnimalsAplysiaBehavior, AnimalBenzophenanthridinesBiophysicsBiotinBrainCell-Penetrating PeptidesCells, CulturedCoculture TechniquesDose-Response Relationship, DrugElectric StimulationEnzyme InhibitorsExcitatory Postsynaptic PotentialsLipopeptidesBenzophenanthridinesBiotinCell-Penetrating PeptideschelerythrineEnzyme InhibitorsLipopeptidesOligonucleotidesProtein Kinase CProtein Kinase InhibitorsSerotoninzeta-inhibitory peptide

Identifiers

PMID21525283
PMCPMC3102530

What OpenQuestion holds

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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.