Evidence map›Paper›PMID 22893682›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

A cellular model of memory reconsolidation involves reactivation-induced destabilization and restabilization at the sensorimotor synapse in Aplysia.

Sue-Hyun Lee, Chuljung Kwak, Jaehoon Shim, Jung-Eun Kim, Sun-Lim Choi, Hyoung F Kim, Deok-Jin Jang, Jin-A Lee, Kyungmin Lee, Chi-Hoon Lee and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 82 citations in OpenAlex.

  1. Engrams of Fear Memory Attenuation.Advances in neurobiology · 2024
    Review
  2. Article
  3. Improvements in operant memory ofFrontiers in behavioral neuroscience · 2023
    Article
  4. Review
  5. Article
  6. Excitatory postsynaptic calcium transients atLearning & memory (Cold Spring Harbor, N.Y.) · 2021
    Article
  7. Memory Destabilization and Reconsolidation Dynamically Regulate the PKMζ Maintenance Mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  8. Is Reconsolidation a General Property of Memory?Frontiers in human neuroscience · 2021
    Review
  9. Balanced actions of protein synthesis and degradation in memory formation.Learning & memory (Cold Spring Harbor, N.Y.) · 2019
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. An Update on Memory Reconsolidation Updating.Trends in cognitive sciences · 2017
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Reconsolidation and the Dynamic Nature of Memory.Cold Spring Harbor perspectives in biology · 2015
    Review
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

15 authors at 8 institutions in 4 countries.

Sue-Hyun LeeDepartment of Biological Sciences, National Creative Research Initiative Center for Memory, College of Natural Sciences, Seoul National University, Seoul 151-747, Korea.
Chuljung Kwak
Jaehoon Shim
Jung-Eun Kim
Sun-Lim Choi
Hyoung F Kim
Deok-Jin Jang
Jin-A Lee
Kyungmin Lee
Chi-Hoon Lee
Young-Don Lee
Maria Concetta Miniaci
Craig H Bailey
Eric R Kandel
Bong-Kiun Kaang
Creative Research · GBJeju National University · KRKyungpook National University · KRHannam University · KRHoward Hughes Medical Institute · USNew York State Psychiatric InstituteSeoul National University · KRUniversity of Naples Federico II · IT

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

The memory reconsolidation hypothesis suggests that a memory trace becomes labile after retrieval and needs to be reconsolidated before it can be stabilized. However, it is unclear from earlier studies whether the same synapses involved in encoding the memory trace are those that are destabilized and restabilized after the synaptic reactivation that accompanies memory retrieval, or whether new and different synapses are recruited. To address this issue, we studied a simple nonassociative form of memory, long-term sensitization of the gill- and siphon-withdrawal reflex in Aplysia, and its cellular analog, long-term facilitation at the sensory-to-motor neuron synapse. We found that after memory retrieval, behavioral long-term sensitization in Aplysia becomes labile via ubiquitin/proteasome-dependent protein degradation and is reconsolidated by means of de novo protein synthesis. In parallel, we found that on the cellular level, long-term facilitation at the sensory-to-motor neuron synapse that mediates long-term sensitization is also destabilized by protein degradation and is restabilized by protein synthesis after synaptic reactivation, a procedure that parallels memory retrieval or retraining evident on the behavioral level. These results provide direct evidence that the same synapses that store the long-term memory trace encoded by changes in the strength of synaptic connections critical for sensitization are disrupted and reconstructed after signal retrieval.

Indexed as

AnimalsAplysiaBehavior, AnimalCells, CulturedCoculture TechniquesElectroshockExcitatory Postsynaptic PotentialsFearGillsMemoryModels, AnimalMotor NeuronsNerve Tissue ProteinsNeuronal PlasticityReflexSensory Receptor CellsNerve Tissue ProteinsSerotoninSerotonin Receptor Agonists

Identifiers

PMID22893682
PMCPMC3435208
OpenAlexW2047758256

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.