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Related Experiment Videos

Cholecystokinin induces a decrease in Ca2+ current in snail neurons that appears to be mediated by protein kinase C.

C Hammond, D Paupardin-Tritsch, A C Nairn

    Nature
    |February 4, 1987
    PubMed
    Summary
    This summary is machine-generated.

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    Cholecystokinin (CCK8) modulates snail neuron calcium currents via protein kinase C activation. This neuropeptide signaling pathway offers new insights into neuronal excitability regulation.

    Area of Science:

    • Neuroscience
    • Molecular Biology
    • Cell Physiology

    Background:

    • Protein kinases regulate Ca2+ currents in excitable cells.
    • Cyclic AMP-dependent and cyclic GMP-dependent protein kinases modulate cardiac and neuronal Ca2+ currents, respectively.
    • Ca2+/diacylglycerol-dependent protein kinase (protein kinase C) regulates neuronal Ca2+ currents, but neurotransmitter activation remains unestablished.

    Purpose of the Study:

    • To investigate the role of cholecystokinin (CCK) in modulating Ca2+ currents in snail neurons.
    • To determine if protein kinase C mediates the effects of CCK on neuronal Ca2+ currents.

    Main Methods:

    • Electrophysiological recordings in identified Helix aspersa neurons.
    • Application of sulphated cholecystokinin octapeptide 26-33 (CCK8).

    Related Experiment Videos

  • Intracellular injection of protein kinase C activators and protein kinase C itself.

    • Main Results:

    • CCK8, protein kinase C activators, and intracellular protein kinase C injection shortened Ca2+-dependent action potentials.
    • These treatments decreased the amplitude of Ca2+ currents, with effects being irreversible within the experimental timeframe.
    • Low concentrations of intracellular protein kinase C enhanced CCK8's effect on Ca2+ current.

    Conclusions:

    • Cholecystokinin (CCK8) modulates Ca2+ currents in Helix aspersa neurons.
    • The neuropeptide's effect is mediated by protein kinase C activation.
    • This study establishes a novel neurotransmitter pathway for protein kinase C-dependent regulation of neuronal excitability.