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A genetic switch for long-term memory

C Pittenger1, E Kandel

  • 1Howard Hughes Medical Institute, Center for Neurobiology and Behavior, Columbia University College, New York, NY 10032, USA.

Comptes Rendus De L'Academie Des Sciences. Serie III, Sciences De La Vie
|October 6, 1998
PubMed
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Learning involves synaptic plasticity, with a late phase requiring gene expression. This phase is regulated by a balance between transcription activators (like ApCREB1) and repressors (like ApCREB2), a mechanism conserved in mice for long-term memory.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Learning and memory involve changes in synaptic efficacy.
  • Synaptic plasticity exhibits early (protein-independent) and late (protein-dependent) phases.
  • Understanding the regulation of the late phase is crucial for comprehending memory formation.

Purpose of the Study:

  • To investigate the regulatory mechanisms of the late phase of synaptic plasticity.
  • To elucidate the role of transcriptional activators and repressors in long-term memory.
  • To examine the conservation of these regulatory mechanisms across species.

Main Methods:

  • Studied synaptic plasticity in Aplysia and mice.
  • Investigated the roles of ApCREB1 (activator) and ApCREB2 (repressor) in Aplysia.

Related Experiment Videos

  • Examined the involvement of CREB in long-term potentiation (LTP) in mice.
  • Main Results:

    • In Aplysia, late-phase synaptic facilitation is controlled by a balance between ApCREB1 and ApCREB2.
    • Perturbing this transcriptional balance initiates the late phase of synaptic plasticity.
    • CREB plays a role in activating genes necessary for LTP in mice, suggesting conserved mechanisms.

    Conclusions:

    • The late phase of synaptic plasticity is initiated by a switch in the balance of transcriptional activators and repressors.
    • This regulatory mechanism appears conserved between Aplysia and mice.
    • A similar balance may regulate genes essential for long-term memory in mammals.