The role of the GluR2 subunit in AMPA receptor function and synaptic plasticity.

By J. Isaac, Michael C. Ashby, C. McBain. Neuron, 2007

809 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/2cde88b802d6f2cf8bbe48df5acf62d01b99fe25

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Citations in the corpus

Sweet Sixteen for ANLS (2012, background): “The AMPA type glutamate receptor subunit GluR2 is known to participate to the mechanism of synaptic plasticity at glutamatergic synapses (Isaac et al, 2007).”
The Self-Tuning Neuron: Synaptic Scaling of Excitatory Synapses (2008, background): “AMPA receptors are heterotetramers composed of subunits GluR1-4 (Greger et al., 2007), and each of these subunits confers different properties on the receptor (Isaac et al., 2007) and can be regulated differently by interactions with scaffolding and signaling molecules (Bredt and Nicoll, 2003).”
Functional Maturation of the First Synapse in Olfaction: Development and Adult Neurogenesis (2008, background): “4), so the AMPA:NMDA ratio increase is also not attributable to a change in AMPA receptor type (Isaac et al., 2007).”
Neurobiology of the incubation of drug craving (2011, unknown): “Physiological differences between GluA2-lacking and GluA2-containing AMPARs in the brain and their relevance for incubation of cocaine craving GluA2-lacking AMPARs differ from GluA2-containing AMPARs in several physiological characteristics, including channel conductance, permeability to calcium ion”
Drug-evoked synaptic plasticity in addiction: from molecular changes to circuit remodeling (2011, unknown): “In fact, pharmacological or synaptic activation of mGluR1 in slices from cocaine-treated mice quickly removes GluA2-lacking AMPARs and replaces them with GluA2-containing ones, leading to an overall depression of synaptic transmission (Bellone and Lüscher, 2005, 2006).”
Calmodulin-Kinases: Modulators of Neuronal Development and Plasticity (2008, unknown): “CaMKK/CaMKI may partially regulate LTP through synaptic trafficking of a special class of AMPARs, calcium-permeable AMPARs (CP-AMPARs) that lack the edited-GluR2 subunit (Isaac et al., 2007).”
Crystal structure of the GluR2 amino-terminal domain provides insights into the architecture and assembly of ionotropic glutamate receptors. (2009, methodology): “In order to gain a mechanistic understanding of ATD functions, we undertook a structural analysis of this region from human GluR2, a subunit of crucial importance for the function of AMPA receptors.(18) A construct containing GluR2 residues 25 to 412 (GluR2-ATD) was expressed in HEK293S-GnTI cells, ”
Glutamate Receptor Ion Channels: Structure, Regulation, and Function (2010, background): “IUPHAR Name HUGO Symbol Common Names Human Chromosome Amino Acids in Longest Splice Variant GluA1 GRIA1 GluR1, GluRA 5q31.”
Projection-specific modulation of dopamine neuron synapses by aversive and rewarding stimuli (2011, unknown): “Because the presence of inwardly rectifying, GluA2-lacking AMPARs can influence the AMPAR/ NMDAR ratios when measured at +40 mV (Isaac et al., 2007), we also calculated the AMPAR/NMDAR ratios based on recording AMPAR EPSCs at −70 mV and NMDAR EPSCs at +40 mV.”