AMPA-type glutamate receptors (AMPARs) mediate most fast excitatory synaptic transmission in the mammalian brain. It is widely believed that the long-lasting, activity-dependent changes in synaptic strength, including long-term potentiation and long-term depression, could be the molecular and cellular basis of experience-dependent plasticities, such as learning and memory. Those changes of synaptic strength are directly related to AMPAR trafficking to and away from the synapse. There are many forms of synaptic plasticity in the mammalian brain, while the prototypic form, hippocampal CA1 long-term potentiation, has received the most intense investigation. After synthesis, AMPAR subunits undergo posttranslational modifications such as glycosylation, palmitoylation, phosphorylation and potential ubiquitination. In addition, AMPAR subunits spatiotemporally associate with specific neuronal proteins in the cell. Those posttranslational modifications and receptor-associated proteins play critical roles in AMPAR trafficking and regulation of AMPAR-dependent synaptic plasticity. Here, we summarize recent studies on posttranslational modifications and associated proteins of AMPAR subunits, and their roles in receptor trafficking and synaptic plasticity.

Keywords:
Long-term potentiation, Memory, Receptor trafficking, Synaptic plasticity, Posttranslational modification, Receptor-associated proteins, PKMζ, PKCι/λ, p62
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© 2007 S. Karger AG, Basel
2007
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