Excitatory interaction between glutamate receptors and protein kinases

Authors

  • T. R. Soderling,

    Corresponding author
    1. Vollum Institute, Oregon Health Sciences University, Portland, Oregon 97201
    • Vollum Institute, Oregon Health Sciences University, Portland, Oregon 97201
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  • S. E. Tan,

    1. Vollum Institute, Oregon Health Sciences University, Portland, Oregon 97201
    Current affiliation:
    1. Department of Psychology, Kaohsiung Medical School, Kaohsiung, Kaohsiung, Taiwan
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  • E. McGlade-McCulloh,

    1. Vollum Institute, Oregon Health Sciences University, Portland, Oregon 97201
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  • H. Yamamoto,

    1. Vollum Institute, Oregon Health Sciences University, Portland, Oregon 97201
    Current affiliation:
    1. Department of Pharmacology, Kumamoto Medical School, Kumamoto, Japan
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  • K. Fukunaga

    1. Vollum Institute, Oregon Health Sciences University, Portland, Oregon 97201
    Current affiliation:
    1. Department of Pharmacology, Kumamoto Medical School, Kumamoto, Japan
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Abstract

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.

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