Excitatory interactions between glutamate receptors and protein kinases

One of the most active areas of neurobiology research concerns mechanisms involved in paradigms of synaptic plasticity. A popular model for cellular learning and memory is long term potentiation (LTP) in hippocampus. 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 postsynaptic density protein at excitatory glutaminergic synapses, can phosphorylate glutamate receptors and enhance ion current flowing through them.