Evidence map›Paper›PMID 26077687›Full record

ArticleLearning & memory (Cold Spring Harbor, N.Y.)2015

Atypical PKCs in memory maintenance: the roles of feedback and redundancy.

Sajiya J Jalil, Todd Charlton Sacktor, Harel Z Shouval

Abstract read
In one paragraph

Article in Learning & memory (Cold Spring Harbor, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. The Roles of Par3, Par6, and aPKC Polarity Proteins in Normal Neurodevelopment and in Neurodegenerative and Neuropsychiatric Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. PKMζ Inhibition Disrupts Reconsolidation and Erases Object Recognition Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Memory Takes Time.Neuron · 2017
    Review
  19. Article
  20. Cell-Specific PKM Isoforms Contribute to the Maintenance of Different Forms of Persistent Long-Term Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    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.

Sajiya J JalilDepartment of Neurobiology and Anatomy, The University of Texas Medical School at Houston, Houston, Texas 77030, USA.
Todd Charlton SacktorDepartment of Physiology, Pharmacology, Anesthesiology, and Neurology, SUNY Downstate Medical Center, Brooklyn, New York 11203, USA.
Harel Z ShouvalDepartment of Neurobiology and Anatomy, The University of Texas Medical School at Houston, Houston, Texas 77030, USA Harel.Shouval@uth.tmc.edu.

Funding

PROTEIN KINASE C ISOZYMES IN HIPPOCAMPAL PLASTICITYR01MH053576 · NIMH · SUNY DOWNSTATE MEDICAL CENTER · PI SACKTOR, TODD C · 2000 to 2014
$4.9M
Regulation and Neural Function of Atypical PKCR37MH057068 · NIMH · SUNY DOWNSTATE MEDICAL CENTER · PI SACKTOR, TODD C · 2011 to 2020
$4.0M
CRCNS: PKMzeta-Dependent Protein Synthesis Maintains Synaptic PlasticityR01DA034970 · NIDA · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI SHOUVAL, HAREL ZEEV · 2012 to 2016
$1.4M
NIDA NIH HHS R01 DA034970NIDA NIH HHS R01 DA034979NIMH NIH HHS 2R37 MH057068NIMH NIH HHS R01 MH053576NIMH NIH HHS R01 MH53576NIMH NIH HHS R37 MH057068
6 · The paper itself

Abstract

Memories that last a lifetime are thought to be stored, at least in part, as persistent enhancement of the strength of particular synapses. The synaptic mechanism of these persistent changes, late long-term potentiation (L-LTP), depends on the state and number of specific synaptic proteins. Synaptic proteins, however, have limited dwell times due to molecular turnover and diffusion, leading to a fundamental question: how can this transient molecular machinery store memories lasting a lifetime? Because the persistent changes in efficacy are synapse-specific, the underlying molecular mechanisms must to a degree reside locally in synapses. Extensive experimental evidence points to atypical protein kinase C (aPKC) isoforms as key components involved in memory maintenance. Furthermore, it is evident that establishing long-term memory requires new protein synthesis. However, a comprehensive model has not been developed describing how these components work to preserve synaptic efficacies over time. We propose a molecular model that can account for key empirical properties of L-LTP, including its protein synthesis dependence, dependence on aPKCs, and synapse-specificity. Simulations and empirical data suggest that either of the two aPKC subtypes in hippocampal neurons, PKMζ and PKCι/λ, can maintain L-LTP, making the system more robust. Given genetic compensation at the level of synthesis of these PKC subtypes as in knockout mice, this system is able to maintain L-LTP and memory when one of the pathways is eliminated.

Indexed as

Models, MolecularModels, NeurologicalAnimalsComputer SimulationFeedback, PhysiologicalHippocampusIsoenzymesKineticsLong-Term PotentiationMemoryNeuronsPhosphorylationProtein BiosynthesisProtein Kinase CIsoenzymesProtein Kinase C

Identifiers

PMID26077687
PMCPMC4478332

What OpenQuestion holds

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LicenceCC BY-NC
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.