Phosphorylation of the AMPA receptor GluR1 subunit is required for synaptic plasticity and retention of spatial memory.

By Hey-Kyoung Lee, K. Takamiya, Jung-Soo Han, Hengye Man, Chong-Hyun Kim, Gavin Rumbaugh, Sandy Yu, Lin Ding, Chun-Wei He, R. Petralia and 3 more. Cell, 2003

832 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Developmental Neuroscience

View Paper: https://www.semanticscholar.org/paper/596fd0d4885e3d07fa4edfa9f71fd6a668dd61c6

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In Cellular and Molecular Neuroscience

In Cognitive Neuroscience

In Developmental Neuroscience

Citations in the corpus

The cell biology of synaptic plasticity: AMPA receptor trafficking. (2007, background): “Mice that have these two sites mutated exhibit major deficits in LTD and AMPAR internalization induced by NMDAR activation (Lee et al. 2003).”
Handbook of ion channels (2015, background): “Knock-in mice with ablated phosphorylation sites in the GluA1 C-terminus (S831A S845A double mutant) lack hippocampal NMDA-receptor-dependent LTD but still exhibited (albeit reduced) LTP (Lee et al., 2003).”
The mGluR theory of fragile X mental retardation. (2004, neutral): “Interestingly, although both forms of hippocampal LTD can be induced by identical patterns of synaptic stimulation [ 21 ,22] and can be expressed as a decrease in the number of postsynaptic AMPA receptors [23,24], they are mechanistically distinct.”
TARP γ-8 controls hippocampal AMPA receptor number, distribution and synaptic plasticity (2005, positive): “Mice lacking the phosphorylation sites on GluR1 that are involved in synaptic plasticity show normal basal synaptic transmissio”
Glutamate Receptor Ion Channels: Structure, Regulation, and Function (2010, background): “In vivo evidence from transgenic animals suggests that GluA1 phosphorylation is critical for synaptic plasticity (Lee et al., 2000, 2003; Whitlock et al., 2006; Tsui and Malenka, 2006).”
Frontiers in Synaptic Neuroscience Synaptic Neuroscience (neutral): “The trafficking of AMPA receptors in and out of the synapse depends on phosphorylation of AMPA receptors at distinct sites (Lee et al., 2000, 2003; Boehm et al., 2006; He et al., 2009).”
Plasticity in the human central nervous system. (2006, background): “, 1988; Malgaroli and Tsien, 1992), with much current work focusing on changes in the intrinsic conductance of glutamate receptor channels (Derkach et al., 1999; Lee et al., 2003) or in the number inserted into the synaptic membrane (Takahashi et al.”
Regulatory mechanisms of AMPA receptors in synaptic plasticity (2007, background): “and is associated with membrane trafficking and phosphorylation of synaptic AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid)-type glutamate receptors (AMPARs”
Modeling the dynamic interaction of Hebbian and homeostatic plasticity. (2014, background): “This weakening shares other molecular features of Hebbian long-term depression (LTD) (Heynen et al., 2003; Yoon et al., 2009) but differs from LTD in its dependence on protein synthesis (Lee et al., 2003; Shepherd and Huganir, 2007; Taha and Stryker, 2002).”
Models and mechanisms of hyperalgesia and allodynia. (2009, background): “Phosphorylation of the GluR1 subunit is an essential step of LTP at glutamatergic synapses (44, 277).”
Structural plasticity and memory (2004, background): “Knock-in mice with mutations in the GluR1 S831 and S845 phosphorylation sites are deficient in NMDA-dependent trafficking of AMPA receptor”
Regulation of AMPA Receptor Trafficking and Synaptic Plasticity (2012, background): “SAP97 also interacts with PKA anchoring molecule AKAP79 [22], which may enhance GluA1 phosphorylation at Ser-845 that can regulate LTP [23].”