Regulatory mechanisms of AMPA receptors in synaptic plasticity

By V. Derkach, Michael C. Oh, Eric S. Guire, T. Soderling. Nature Reviews Neuroscience, 2007

762 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/aed1365153fe981e5b8af2fa992458f03832fc0e

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Citations in the corpus

Frontiers in Synaptic Neuroscience Synaptic Neuroscience (neutral): “For example, dopamine D1/D5 receptors and β-adrenergic receptors can increase surface expression of AMPA receptors (Chao et al., 2002; Sun et al., 2005; Oh et al., 2006) promoting synaptic insertion (for reviews see: Derkach et al., 2007; Lee and Huganir, 2008).”
From synapse to nucleus: calcium-dependent gene transcription in the control of synapse development and function. (2008, background): “A similar process of synapse elimination occurs in the CNS (e.g., the retinogeniculate synapse, the synapse made by retinal ganglion neurons onto thalamic neurons, and the climbing fiber/Purkinje cell synapse in the cerebellum) (Chen and Regehr, 2000; Nishiyama and Linden, 2004).”
Glutamate Receptor Ion Channels: Structure, Regulation, and Function (2010, background): “Considerably more work will be required before we achieve adequate understanding of the relative contribution of phosphorylation-linked changes in trafficking and channel function to changes in synaptic strength (Song and Huganir, 2002; Derkach et al., 2007; Kessel and Malinow., 2009) (see sections ”
Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms (2008, background): “Although these subunits are highly homologous, both the functional properties of AMPARs and their trafficking has been suggested to depend on their subunit composition (Collingridge et al, 2004; Derkach et al, 2007; Malinow and Malenka, 2002).”
BDNF: A Key Factor with Multipotent Impact on Brain Signaling and Synaptic Plasticity (2017, background): “In contrast, pro-BDNF expressed during low-frequency stimulation has been reported to induce LTD (Woo et al. 2005; Yang et al. 2014).”
Calmodulin-Kinases: Modulators of Neuronal Development and Plasticity (2008, neutral): “…throughout the brain, but the focus here will be the CA1 synapse in the hippocampus where long-term potentiation (LTP) and depression (LTD), cellular models of learning and memory, have been most intensively investigated (reviewed in Derkach et al., 2007; Lisman et al., 2002; Luscher et al., 2000).”
Pathways and mechanisms of endocytic recycling (2009, neutral): “Spines increase in membrane area and in the number of surface-resident AMPARs (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors) in response to NMDAR ( N -methyl- D -aspartate receptor) activation during long-term potentiation, and both of these acute changes depend on RAB11- and EHD1”
Dendritic mRNA: transport, translation and function (2007, background): “Arc and LIMK1 are both implicated in the local regulation of actin dynamics that underlies the remodelling of spines, whereas αCaMKII and PKMζ are key regulators of AMPA-receptor-trafficking and activit”
Mechanisms of CaMKII action in long-term potentiation (2012, background): “Interestingly, for AMPARs containing both GluR1 and GluR2, the ability of S831 phosphorylation to increase channel conductance only occurs if stargazin is presen”
NMDA receptor trafficking in synaptic plasticity and neuropsychiatric disorders (2007, background): “The prevailing view is that NMDARs function as the trigger of LTP and LTD and that the primary expression mechanism of synaptic plasticity involves alterations in the number, phosphorylation stat”