Activation of Ca2+/calmodulin-dependent protein kinase II in cerebellar granule cells by N-methyl-d-aspartate receptor activation

Koji Fukunaga, Thomas R. Soderling

    Research output: Contribution to journalArticle

    36 Scopus citations

    Abstract

    Cultured cerebellar granule cells were studied to determine if the excitatory neurotransmitter glutamate acting through the N-methyl-d-aspartate (NMDA) receptor could stimulate autophosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaM-kinase II) to generate its Ca2+-independent form. Glutamate did elevate Ca2+-independent CaM-kinase II through autophosphorylation when granule cells were incubated in Mg2+-free buffer, and this response was potentiated by 1 μM glycine. Extracellular Ca2+ was required, and specific antagonists of the NMDA receptor blocked the response. These results support the hypothesis that postsynaptic Ca2+ influx through the NMDA receptor-gated ion channel, as occurs during induction of long-term potentiation, may convert CaM-kinase II to a constitutively active, Ca2+-independent form.

    Original languageEnglish (US)
    Pages (from-to)133-138
    Number of pages6
    JournalMolecular and Cellular Neuroscience
    Volume1
    Issue number2
    DOIs
    StatePublished - Oct 1990

    ASJC Scopus subject areas

    • Molecular Biology
    • Cellular and Molecular Neuroscience
    • Cell Biology

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