期刊
NEUROSIGNALS
卷 15, 期 5, 页码 266-282出版社
KARGER
DOI: 10.1159/000105517
关键词
long-term potentiation; memory; receptor trafficking; synaptic plasticity; posttranslational modification; receptor-associated proteins; PKM zeta; PKC iota/lambda; p62
资金
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS033661] Funding Source: NIH RePORTER
- NINDS NIH HHS [NS33661] Funding Source: Medline
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. Copyright (c) 2007 S. Karger AG, Basel.
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