PKA phosphorylation of AMPA receptor subunits controls synaptic trafficking underlying plasticity

By J. Esteban, S. Shi, Christopher L. Wilson, Mutsuo Nuriya, Richard L. Huganir, R. Malinow. Nature Neuroscience, 2003

895 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience

View Paper: https://www.semanticscholar.org/paper/768b4aaad1b952ce74a5f1832b8aa3916bb476c0

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

In Cognitive Neuroscience

Citations in the corpus

Structural plasticity and memory (2004, background): “For example, phosphorylation of GluR1 at S845 by protein kinase A (PKA) is necessary (although not sufficient) for the delivery of GluR1 into synapse”
Neuronal circuitry for pain processing in the dorsal horn (2010, background): “Hippocampal LTP is thought to involve insertion of AMPARs containing either GluA1 or GluA4 subunits into glutamatergic synapses, leading to increased postsynaptic responses to glutamat”
Making memories last: the synaptic tagging and capture hypothesis (2010, background): “Thus, the expression of E-LTP is mediated in part by the synaptic incorporation of additional AMPAR”
AKAP signalling complexes: focal points in space and time (2004, background): “Not only do the two slightly different configurations ( Fig 4a,b ) contribute to the efficiency of PKA-phosphorylation events, but they also maintain the protein phosphatase PP2B in proximity to its substrates so that it can oppose the actions of PK”
Rapid and persistent modulation of actin dynamics regulates postsynaptic reorganization underlying bidirectional plasticity (2004, neutral): “For instance, AMPA receptor subunits require direct phosphorylation for targeting to the synapse, but this alone is not sufficient for translocatio”
NMDA receptor subunit composition controls synaptic plasticity by regulating binding to CaMKII. (2005, neutral): “At early postnatal stages (before postnatal day 9 [P9]), potentiation-inducing stimuli act through PKA (Esteban et al., 2003; Yasuda et al., 2003) to drive GluR4-containing AMPA receptors (AMPA-Rs) into synapses (Zhu et al., 2000) and enhance transmission.”
Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms (2008, background): “Phosphorylation of AMPAR subunits themselves by CaMKII does not appear critical (Esteban et al, 2003; Lee et al, 2003) although other phosphorylation sites, such as the PKA or the PKC sites on GluR1, may be important (Boehm et al, 2006; Esteban et al, 2003).”
Assembly of a β2‐adrenergic receptor—GluR1 signalling complex for localized cAMP signalling (2010, methodology): “…of AMPARs on LTP. Phosphorylation of GluR1 by PKA on serine 845 (S845) is critical for activity-driven accumulation of GluR1 at postsy- naptic sites (Esteban et al, 2003) and fosters surface expression of GluR1 (Ehlers, 2000; Swayze et al, 2004; Sun et al, 2005; Oh et al, 2006; Man et al, 2007).”
Glutamate Receptor Ion Channels: Structure, Regulation, and Function (2010, background): “GluA4 has alternate C-tails, with the short tail terminated by a PKC target at TES899IK (Esteban et al., 2003).”