ABSTRACT
Plasticity of excitatory synapses is believed to underlie important aspects of signal integration by neuronal networks. Until recently, plasticity was essentially considered in terms of functional changes in the efficacy of transmission, focusing particularly on long-term potentiation (LTP), an increase in synaptic strength induced by a brief period of high frequency stimulation (1). Decades of intense research on the molecular mechanisms contributing to this form of plasticity have revealed the central role played by postsynaptic receptors in this process (1-4). Following activation of NMDA receptors during high frequency stimulation, calcium triggers signaling cascades that modify the properties or number of postsynaptic AMPA type receptors expressed at the synaptic membrane (5-8). Phosphorylation-dependent mechanisms that affect receptor properties and recycling or diffusion in the membrane appear therefore to be critically implicated in the changes of synaptic efficacy.
