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Long-term potentiation: persisting problems and recent results.

G Lynch1, D Muller, P Seubert

  • 1Center for the Neurobiology of Learning and Memory, University of California, Irvine 92717.

Brain Research Bulletin
|September 1, 1988
PubMed
Summary
This summary is machine-generated.

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Long-term potentiation (LTP) involves calcium influx, dendritic spine changes, and potentially new synapses. Calpain activation is crucial for LTP, suggesting a role in memory encoding.

Area of Science:

  • Neuroscience
  • Cellular Biology
  • Molecular Biology

Background:

  • Long-term potentiation (LTP) is a key mechanism for synaptic plasticity.
  • Unresolved issues include the enduring substrates, biochemical mechanisms, and memory role of LTP.

Purpose of the Study:

  • To review experimental results on LTP substrates, mechanisms, and memory functions.
  • To investigate the role of calcium, protein kinase C, and calpain in LTP.
  • To explore LTP's contribution to learning in cortical networks.

Main Methods:

  • Analysis of experimental data on LTP.
  • Investigating the effects of calcium influx, protein kinase C, and calpain inhibitors (leupeptin).
  • Examining NMDA receptor activation and spectrin proteolysis.

Related Experiment Videos

  • Computer simulations of cortical networks.

    • Main Results:

    • LTP is triggered by postsynaptic calcium influx, affecting dendritic spines and synapse formation.
    • Presynaptic calcium currents are not associated with LTP.
    • Calpain activation is pivotal for LTP, as shown by leupeptin blocking.
    • NMDA receptor activation leads to calcium-sensitive spectrin proteolysis.
    • Naturalistic stimulation patterns effectively induce LTP.

    Conclusions:

    • Calpain activation is essential for establishing LTP.
    • LTP likely occurs during information encoding in cortical systems.
    • LTP may contribute significantly to learning and memory processes.