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Dendritic K+ channels contribute to spike-timing dependent long-term potentiation in hippocampal pyramidal neurons

  1. Daniel Johnston*‖
  1. *Division of Neuroscience, Baylor College of Medicine, Houston, TX 77030; and §Department of Neurobiology, Yale University School of Medicine, New Haven, CT 06520-8001

  1. Communicated by Bert Sakmann, Max Planck Institute for Medical Research, Heidelberg, Germany (received for review February 8, 2002)

Abstract

We investigated the role of A-type K+ channels for the induction of long-term potentiation (LTP) of Schaffer collateral inputs to hippocampal CA1 pyramidal neurons. When low-amplitude excitatory postsynaptic potentials (EPSPs) were paired with two postsynaptic action potentials in a theta-burst pattern, N-methyl-d-aspartate (NMDA)-receptor-dependent LTP was induced. The amplitudes of the back-propagating action potentials were boosted in the dendrites only when they were coincident with the EPSPs. Mitogen-activated protein kinase (MAPK) inhibitors PD 098059 or U0126 shifted the activation of dendritic K+ channels to more hyperpolarized potentials, reduced the boosting of dendritic action potentials by EPSPs, and suppressed the induction of LTP. These results support the hypothesis that dendritic K+ channels and the boosting of back-propagating action potentials contribute to the induction of LTP in CA1 neurons.

Footnotes

    • ↵† Present address: Department of Physiology, New York Medical College, Valhalla, NY 10595.

    • ↵‡ Present address: Max Planck Institute for Medical Research, Jahnstrasse 29, D-69120 Heidelberg, Germany.

    • ↵ Permanent address: National Research Council, Institute of Advanced Diagnostic Methodologies, 90146 Palermo, Italy.

    • ↵‖ To whom reprint requests should be addressed. E-mail: dan{at}mossy.bcm.tmc.edu.

  • Abbreviations

    LTP,
    long-term potentiation;
    EPSP,
    excitatory postsynaptic potential;
    NMDA,
    N-methyl-d-aspartate;
    APV,
    dl-2-amino-5-phosphonovaleric acid;
    TBP,
    theta-burst pairing;
    MAPK,
    mitogen-activated protein kinase;
    MEK,
    MAPK kinase;
    ERK,
    extracellular signal-regulated kinase
    • Received February 8, 2002.
    • Accepted April 8, 2002.

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