Excitatory interaction between glutamate receptors and protein kinases
Article first published online: 11 OCT 2004
Copyright © 1994 John Wiley & Sons, Inc.
Journal of Neurobiology
Volume 25, Issue 3, pages 304–311, March 1994
How to Cite
Soderling, T. R., Tan, S. E., McGlade-McCulloh, E., Yamamoto, H. and Fukunaga, K. (1994), Excitatory interaction between glutamate receptors and protein kinases. J. Neurobiol., 25: 304–311. doi: 10.1002/neu.480250310
- Issue published online: 11 OCT 2004
- Article first published online: 11 OCT 2004
- Manuscript Accepted: 15 SEP 1993
- Manuscript Received: 20 AUG 1993
- glutamate receptors;
- synaptic plasticity;
- protein kinases
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.