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Role of protein synthesis and DNA methylation in the consolidation and maintenance of long-term memory in Aplysia

  1. Kaycey Pearce
  2. Diancai Cai
  3. Adam C Roberts
  4. David L Glanzman  Is a corresponding author
  1. Univeristy of California, Los Angeles, United States
Research Article
  • Cited 23
  • Views 1,780
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Cite this article as: eLife 2017;6:e18299 doi: 10.7554/eLife.18299

Abstract

Previously, we reported that long-term memory (LTM) in Aplysia can be reinstated by truncated (partial) training following its disruption by reconsolidation blockade and inhibition of PKM (Chen et al., 2014). Here, we report thatLTM can be induced by partial training after disruption of original consolidation by protein synthesis inhibition (PSI) begun shortly after training. But when PSI occurs during training, partial training cannot subsequently establish LTM. Furthermore, we find that inhibition of DNA methyltransferase (DNMT), whether during training or shortly afterwards, blocks consolidation of LTM and prevents its subsequent induction by truncated training; moreover, later inhibition of DNMT eliminates consolidated LTM. Thus, the consolidation of LTM depends on two functionally distinct phases of protein synthesis: an early phase that appears to prime LTM; and a later phase whose successful completion is necessary for the normal expression of LTM. Both the consolidation and maintenance of LTM depend on DNA methylation.

Article and author information

Author details

  1. Kaycey Pearce

    Department of Integrative Biology and Physiology, Univeristy of California, Los Angeles, Los Angeles, United States
    Competing interests
    The authors declare that no competing interests exist.
  2. Diancai Cai

    Department of Integrative Biology and Physiology, Univeristy of California, Los Angeles, Los Angeles, United States
    Competing interests
    The authors declare that no competing interests exist.
  3. Adam C Roberts

    Department of Integrative Biology and Physiology, Univeristy of California, Los Angeles, Los Angeles, United States
    Competing interests
    The authors declare that no competing interests exist.
  4. David L Glanzman

    Department of Integrative Biology and Physiology, Univeristy of California, Los Angeles, Los Angeles, United States
    For correspondence
    glanzman@ucla.edu
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-5479-0245

Funding

National Institute of Neurological Disorders and Stroke (NIH R01 NS029563)

  • David L Glanzman

National Institute of Mental Health (NIH R01 MH096120)

  • David L Glanzman

National Science Foundation (IOS 1121690)

  • David L Glanzman

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

  1. Mani Ramaswami, Trinity College Dublin, Ireland

Publication history

  1. Received: June 1, 2016
  2. Accepted: January 7, 2017
  3. Accepted Manuscript published: January 9, 2017 (version 1)
  4. Accepted Manuscript updated: January 10, 2017 (version 2)
  5. Version of Record published: February 15, 2017 (version 3)

Copyright

© 2017, Pearce et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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