AMPA receptor trafficking and synaptic plasticity.

By R. Malinow, R. Malenka. Annual Review of Neuroscience, 2002

2,707 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/0441e81d3b9b48095e5cd9d08c3eb58f9003388d

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Citations in the corpus

Central sensitization and LTP: do pain and memory share similar mechanisms? (2003, methodology): “Similarities and differences between mechanisms of central sensitization and hippocampal LTP Resemblance between the early phase of CA1 hippocampal LTP and activity-dependent classical central sensitization The postsynaptic mechanisms responsible for the induction and expression of the early phase o”
Impact of aging on hippocampal function: plasticity, network dynamics, and cognition. (2003, background): “, 1996, 2000; Manahan-Vaughan, 1997) has shown that, under certain conditions, reductions in synaptic strength can be induced both in vitro and in vivo (for reviews, see Bear and Abraham, 1996; Kemp and Bashir, 2001; Malinow and Malenka, 2002).”
Addiction: a disease of learning and memory. (2005, background): “Molecular mechanisms underlying long-term potentiation and long-term depression include regulation of the phosphorylation state of key proteins, alterations in the availability of glutamate receptors at the synapse, and regulation of gene expression (78, 82).”
Compartmentalizing the neuronal plasma membrane from axon initial segments to synapses. (2009, background): “Transport of NMDAR and AMPAR is regulated by interaction with proteins like PDZ domain proteins, chaperones, endocytic adaptors, and cytoskeleton (Bredt and Nicoll, 2003; Malinow and Malenka, 2002; Wenthold et al., 2003).”
Abundant distribution of TARP γ‐8 in synaptic and extrasynaptic surface of hippocampal neurons and its major role in AMPA receptor expression on spines and dendrites (2006, background): “…dynamic changes by endocytosis–exocytosis and by lateral movement from extrasynaptic to synaptic sites, which are thought to underlie activitydependent neural plasticity and developmental synapse maturation (Sheng & Lee, 2001; Malinow & Malenka, 2002; Song & Huganir, 2002; Bredt & Nicoll, 2003).”
Ubiquitination regulates PSD-95 degradation and AMPA receptor surface expression. (2003, background): “reserve insertion sites for AMPA receptors at the synapse (Malinow and Malenka, 2002; Shi et al., 2001).”
Dendritic excitability and synaptic plasticity. (2008, positive): “In addition, Bloodgood and Sabatini (78) propose that this mechanism may form a novel substrate for LTP and LTD, since it suggests synaptic strength theoretically can be regulated independently of either AMPA receptor regulation (193, 368, 415, 424, 452, 482, 700, 812) or presynaptic changes in neur”
Regulatory mechanisms of AMPA receptors in synaptic plasticity (2007, background): “Although these subunits are highly homologous, both the functional properties of AMPARs and their trafficking depend on subunit compositio”
Homeostatic plasticity in the developing nervous system (2004, background): “Rapid insertion of AMPARs contributes to the increase in synaptic transmission induced by some LTP protocol”
Functional Maturation of the First Synapse in Olfaction: Development and Adult Neurogenesis (2008, background): “Identical increases in AMPA:NMDA ratio at maturing ON synapses in postnatal development and adult neurogenesis In many areas of the brain, immature glutamatergic synapses are characterized by a relative predominance of NMDA over AMPA receptors, which switches to a predominance of AMPA over NMDA rece”
The spike timing dependence of plasticity (2012, background): “The primary expression mechanisms are postsynaptic, via addition or removal of postsynaptic AMPA receptors (AMPARs) and changes in single-channel conductance (Malinow and Malenka, 2002), though presynaptic expression can also occur.”