CaM-kinases: Modulators of synaptic plasticity

Thomas R. Soderling

    Research output: Contribution to journalReview article

    190 Scopus citations

    Abstract

    Calcium signaling is crucial for several aspects of plasticity at glutamatergic synapses, and studies over the past two to three years have identified key functions for Ca2+/calmodulin-dependent protein kinases II and IV (CaM-KII and CaM-KIV). Sustained activation of CaM-KII localized at the postsynaptic density results in phosphorylation of numerous synaptic substrates including ion channels, other signaling molecules and scaffolding proteins, to modulate synaptic transmission within minutes. More prolonged responses may be effected through enhanced dendritic protein synthesis of CaM-KII and regulation of nuclear gene transcription by CaM-KIV.

    Original languageEnglish (US)
    Pages (from-to)375-380
    Number of pages6
    JournalCurrent Opinion in Neurobiology
    Volume10
    Issue number3
    DOIs
    StatePublished - Jun 1 2000

    ASJC Scopus subject areas

    • Neuroscience(all)

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