title: AMPA receptor trafficking and learning.
abstract: In the last few years it has become clear that AMPA-type glutamate neurotransmitter receptors are rapidly transported into and out of synapses to strengthen or weaken their function. The remarkable dynamics of AMPA receptor (AMPAR) synaptic localization provides a compelling mechanism for understanding the cellular basis of learning and memory, as well as disease states involving cognitive dysfunction. Here, we summarize the evidence for AMPAR trafficking as a mechanism underlying a variety of learned responses derived from both behavioral and cellular studies. Evidence is also reviewed supporting synaptic dysfunction related to impaired AMPAR trafficking as a mechanism underlying learning and memory deficits in Alzheimer's disease. We conclude that emerging data support the concept of multistage AMPAR trafficking during learning and that a broad approach to include examination of all of the AMPAR subunits will provide a more complete view of the mechanisms underlying multiple forms of learning.
authors.affiliation: Neuroscience Group, Division of Basic Biomedical Sciences, University of South Dakota, Sanford School of Medicine, Vermillion, SD 57069, USA. jkeifer@usd.edu
authors.forename: J
authors.initials: J
authors.lastname: Keifer
authors.forename: Z
authors.initials: Z
authors.lastname: Zheng
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology; D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007858:Learning / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D021381:Protein Transport / Q000502:physiology; D018091:Receptors, AMPA / Q000378:metabolism*; D013569:Synapses / Q000378:metabolism / Q000473:pathology; D009435:Synaptic Transmission / Q000502:physiology
chemical_list: D018091:Receptors, AMPA