Subunit-specific rules governing AMPA receptor trafficking to synapses in hippocampal pyramidal neurons.
By S. Shi, Yasunori Hayashi, J. Esteban, R. Malinow. Cell, 2001
1,145 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience
View Paper: https://www.semanticscholar.org/paper/8d6e7fd5e650081d7976bf148ff5bea967ffd544
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In Cellular and Molecular Neuroscience
In Cognitive Neuroscience
- Gina G. Turrigiano
- Y. Dudai
- D. Feldman
- R. Malenka
- Richard L. Huganir
- E. Kandel
- Wulfram Gerstner
- M. Mayford
Citations in the corpus
- Hippocampal LTP is accompanied by enhanced F-actin content within the dendritic spine that is essential for late LTP maintenance in vivo. (2003, background): “We found that a strong HFS that elicitsal., 1998; Sheng et al., 2001; Shi et al., 1999, 2001).”
- AMPARs and synaptic plasticity: the last 25 years. (2013, positive): “trafficking of AMPARs is subunit dependent with GluA1/2 heteromers being recruited to spines after LTP, while Glu2/3 heteromers are recruited to synapses in a constitutive manner (Shi et al., 2001).”
- PKA phosphorylation of AMPA receptor subunits controls synaptic trafficking underlying plasticity (2003, background): “These subunits contain either long (GluR1 and GluR4) or short (GluR2 and GluR3) cytoplasmic carboxyl termini that control their trafficking to synapse”
- Synaptic Mechanisms for Plasticity in Neocortex (2009, background): “When GluR1 is overexpressed, LTP causes synaptic insertion of GluR1-homomeric (GluR2-lacking) AMPA receptors, which show unusually high current rectification, allowing LTP to be detected electrophysiologically (Shi et al. 2001).”
- The cell biology of synaptic plasticity: AMPA receptor trafficking. (2007, background): “Recent experiments have shown that endogenous AMPARs can be driven into the synapse during LTP (Shi et al. 2001) and by experience (Takahashi et al. 2003).”
- Structural plasticity and memory (2004, background): “Other studies have indicated that the elevated level of AMPA receptors in the synapse is maintained by an ongoing mechanism that is responsible for the enduring replacement of the additional GluR1/4 receptors with GluR2/3-containing receptors, thereby outlasting protein degradatio”
- The molecular basis of CaMKII function in synaptic and behavioural memory (2002, background): “, a process that depends on the identity of the subunit involve”
- AMPA receptor trafficking at excitatory synapses. (2003, neutral): “conet al., 2001; Piccini and Malinow, 2002; Shi et al., 2001).”
- Ras and Rap control AMPA receptor trafficking during synaptic plasticity. (2002, background): “This AMPA receptor shows rectification and can replace of LTP and LTD, NMDA receptors are activated and the ensuing postsynaptic calcium rise is thought to triggerthe endogenous cycling pool of receptors; thus, the cycling pool of receptors is tagged electrophysiologi- biochemical reactions that eve”
- Subunit-specific temporal and spatial patterns of AMPA receptor exocytosis in hippocampal neurons (2001, background): “Long term potentiation (LTP) in the hippocampus, on the other hand, is correlated with a recruitment of AMPA receptors to the postsynaptic membran”
- The molecular and systems biology of memory. (2014, positive): “…phase of LTP involves activation of second messengers that leads to an increase in the incorporation of new AMPA type glutamate receptors into the synapse resulting in a strengthened response (Hayashi et al., 2000; Shi et al., 2001; Shi et al., 1999; Granger et al., 2013; Malinow et al., 2000).”
- The Self-Tuning Neuron: Synaptic Scaling of Excitatory Synapses (2008, neutral): “…one form of cortical LTP in vitro (Kaneko et al., 2008), but it is not possible to rule out effects on the many other forms of Hebbian or homeostatic plasticity that have been identified in cortical neurons (Abbott and Nelson, 2000; Desai, 2003; Maffei and Turrigiano, 2008; Sjostrom et al., 2006).”
- Homeostatic plasticity in the developing nervous system (2004, background): “These receptors are then replaced with receptors composed of GluR2/3 subunits through constitutive receptor turnove”