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Related Experiment Videos

Increasing Ca2+ transients by broadening postsynaptic action potentials enhances timing-dependent synaptic

Yu-Dong Zhou1, Corey D Acker, Theoden I Netoff

  • 1Department of Biomedical Engineering, Center for Biodynamics, Center for Memory and Brain, Boston University, Boston, MA 02215, USA.

Proceedings of the National Academy of Sciences of the United States of America
|December 21, 2005
PubMed
Summary

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Altering action potential (AP) width in entorhinal cortex (EC) pyramidal cells shifts spike-timing-dependent plasticity (STDP) towards long-term depression (LTD). This finding challenges calcium-peak-detector models and suggests AP width modulates synaptic plasticity rules.

Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Computational Neuroscience

Background:

  • Spike-timing-dependent plasticity (STDP) governs synaptic strength based on the precise timing of pre- and postsynaptic action potentials (APs).
  • Existing models propose that STDP outcomes (LTP/LTD) are determined by calcium transient peaks, influenced by AP timing.
  • The role of AP shape in modulating STDP remains incompletely understood.

Purpose of the Study:

  • To investigate the impact of altered action potential (AP) width on spike-timing-dependent plasticity (STDP) in entorhinal cortex (EC) pyramidal cells.
  • To test the predictions of calcium-peak-detector models of STDP.
  • To explore the mechanisms underlying AP width-dependent modulation of synaptic plasticity.

Main Methods:

  • Electrophysiological recordings in layer II/III pyramidal cells of the entorhinal cortex (EC).

Related Experiment Videos

  • Induction of pre- and postsynaptic activity to induce STDP.
  • Pharmacological manipulation using nifedipine (a Ca(V)1 calcium channel blocker).
  • Analysis of dendritic calcium transients and their correlation with STDP outcomes.

    • Main Results:

    • Broadened APs in EC pyramidal cells increased dendritic calcium transients.
    • Broadened APs shifted the balance of STDP towards long-term depression (LTD).
    • STDP in these cells is NMDA-receptor-dependent and modulated by nifedipine, suggesting Ca(V)1 channel involvement.

    Conclusions:

    • The study challenges simple calcium-peak-detector models by demonstrating that AP width significantly influences STDP.
    • Downstream signaling from voltage-dependent calcium channels appears to suppress long-term potentiation (LTP) relative to LTD.
    • Modulating AP width offers a potent mechanism for adjusting the rules of synaptic plasticity in the entorhinal cortex.