Regulation of distinct AMPA receptor phosphorylation sites during bidirectional synaptic plasticity
By Hey-Kyoung Lee, M. Barbarosie, K. Kameyama, Mark F. Bear, Richard L. Huganir. Nature, 2000
1,181 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience
View Paper: https://www.semanticscholar.org/paper/a8f7bcd157e3618d0dc3395365d6f33ec41500fa
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
- R. Malenka
- Richard L. Huganir
- A. Citri
- Gina G. Turrigiano
- R. Malinow
- J. Shepherd
- Michael D. Ehlers
- T. Soderling
In Cognitive Neuroscience
- R. Malenka
- Richard L. Huganir
- A. Citri
- Richard G. M. Morris
- Wulfram Gerstner
- Michael D. Ehlers
- Guy O. Billings
- R. Malinow
Citations in the corpus
- The cell biology of synaptic plasticity: AMPA receptor trafficking. (2007, background): “However, CaMKII does not seem to be required for synaptic delivery of receptors (Hayashi et al. 2000), although this site is phosphorylated during LTP (Lee et al. 2000).”
- Frontiers in Synaptic Neuroscience Synaptic Neuroscience (positive): “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).”
- 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).”
- PKA phosphorylation of AMPA receptor subunits controls synaptic trafficking underlying plasticity (2003, background): “and has been correlated with changes in synaptic strengt”
- State Based Model of Long-Term Potentiation and Synaptic Tagging and Capture (2009, background): “Although all synapses are initially moved into the strong basal state by the HFS, (resulting briefly in zero fEPSP variability), while the tag-forming reaction in the PSD is still incomplete, a variable number of synapses drop into the weak basal state from where they can no longer access the e-LTP ”
- Single cocaine exposure in vivo induces long-term potentiation in dopamine neurons (2001, result): “This result suggests that cocaine induces either post-translational redistribution of existing AMPARs or phosphorylation of membrane AMPARs, similar to that seen during LTP in hippocampal neuron”
- The molecular basis of CaMKII function in synaptic and behavioural memory (2002, background): “With the development of specific antibodies against GluR1 phosphorylated at Ser831, it became possible to show that LTP increased receptor phosphorylation 30 minutes after LTP induction, with a further increase by one hou”
- Long-term depression in the nucleus accumbens: a neural correlate of behavioral sensitization to cocaine (2001, background): “, a form of synaptic plasticity that is associated with a reduction in AMPAR function and numbe”
- Handbook of ion channels (2015, background): “Serial induction of LTP and LTD and vice versa indicates that the biochemical changes underlying plasticity are reversible (Lee et al., 2000), but the changes in the degree of receptor phosphorylation in these experiments were small, mainly because only a subset of synapses underwent plasticity.”