Excitatory interaction between glutamate receptors and protein kinases

T. R. Soderling, S. E. Tan, E. McGlade‐McCulloh, H. Yamamoto, K. Fukunaga

    Research output: Contribution to journalArticle

    49 Scopus citations


    One of the most active areas of neurobiology research concerns mechanisms involved in paradigms of synaptic plasticity. A popular model for cellular leaning and memory is long term potentiation (LTP) in hippocamus. LTP requires postsynaptic influx of Ca2+ which triggers multiple biochemical pathways resulting in pre‐ and postsynaptic mechanisms enhancing long term synaptic efficiency. This article focuses on an acute postsynaptic Mechanism that can enhance responsiveness of glutamate receptors. Evidence is presented that calcium/calmodulin/dependent protein kinase II, the major potsynaptic density protein at excitatory glutaminergic synapses, can phosphorylate glutamate receptors and enhance ion current flowing through them. 1994 John Wiley & Sons, Inc.

    Original languageEnglish (US)
    Pages (from-to)304-311
    Number of pages8
    JournalJournal of Neurobiology
    Issue number3
    StatePublished - Mar 1994



    • glutamate receptors
    • protein kinases
    • synaptic plasticity

    ASJC Scopus subject areas

    • Neuroscience(all)
    • Cellular and Molecular Neuroscience

    Cite this

    Soderling, T. R., Tan, S. E., McGlade‐McCulloh, E., Yamamoto, H., & Fukunaga, K. (1994). Excitatory interaction between glutamate receptors and protein kinases. Journal of Neurobiology, 25(3), 304-311. https://doi.org/10.1002/neu.480250310