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Histamine and noradrenaline decrease calcium-activated potassium conductance in hippocampal pyramidal cells.

H L Haas, A Konnerth

    Nature
    |March 6, 1983
    PubMed
    Summary
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    Histamine and noradrenaline rapidly decrease the late afterhyperpolarization (AHP) in hippocampal neurons. This modulation by histamine (H2 receptors) and noradrenaline (beta-receptors) enhances neuronal excitability.

    Area of Science:

    • Neuroscience
    • Neurophysiology
    • Cellular Neuroscience

    Background:

    • Histaminergic and noradrenergic systems extensively project to the hippocampus.
    • These amines modulate hippocampal principal neurons via various mechanisms.
    • The late afterhyperpolarization (AHP) in CA1 pyramidal cells, dependent on calcium-activated potassium channels, is influenced by neurotransmitters like dopamine.

    Purpose of the Study:

    • To investigate the rapid effects of histamine and noradrenaline on the late AHP component in hippocampal CA1 pyramidal cells.
    • To elucidate the receptor mechanisms underlying these modulatory actions.

    Main Methods:

    • Perfusion of hippocampal slices with micromolar concentrations of histamine and noradrenaline.
    • Recording of action potentials and afterhyperpolarizations in CA1 pyramidal neurons.

    Related Experiment Videos

  • Electrophysiological analysis to assess changes in the late AHP component and calcium spikes.

    • Main Results:

    • Histamine and noradrenaline induced a rapid and reversible decrease in the late AHP following bursts of sodium or calcium spikes.
    • The effect of histamine was mediated by H2 receptors, while noradrenaline acted via beta-receptors.
    • These modulatory effects occurred without altering the calcium spike itself.

    Conclusions:

    • Histamine and noradrenaline significantly reduce the late AHP in hippocampal CA1 pyramidal neurons.
    • This reduction is mediated by specific receptor pathways (H2 and beta-receptors).
    • By decreasing the late AHP, histamine and noradrenaline can enhance the excitatory impact of depolarizing inputs, thereby potentiating neuronal signaling.