EXCITATORY INTERACTIONS BETWEEN GLUTAMATE RECEPTORS AND PROTEIN-KINASES

One of the most active areas of neurobiology research concerns mechani sms involved in paradigms of synaptic plasticity. A popular model for cellular learning and memory is long term potentiation (LTP) in hippoc ampus. LTP requires postsynaptic influx of Ca2+ which triggers multipl e biochemical pathways resulting in pre- and postsynaptic mechanisms e nhancing long term synaptic efficiency. This article focuses on an acu te postsynaptic mechanism that can enhance responsiveness of glutamate receptors. Evidence is presented that calcium/calmodulin-dependent pr otein kinase II, the major postsynaptic density protein at excitatory glutaminergic synapses, can phosphorylate glutamate receptors and enha nce ion current flowing through them. (C) 1993 John Wiley & Sons, Inc.