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 journalArticlepeer-review

49 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)304-311
Number of pages8
JournalJournal of Neurobiology
Volume25
Issue number3
DOIs
Publication statusPublished - 1994 Mar
Externally publishedYes

Keywords

  • glutamate receptors
  • protein kinases
  • synaptic plasticity

ASJC Scopus subject areas

  • Neuroscience(all)
  • Cellular and Molecular Neuroscience

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