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Synaptic incorporation of AMPA receptors during LTP is controlled by a PKC phosphorylation site on GluR1

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Boehm, Jannic, Kang, Myoung-Goo, Johnson, Richard C., Esteban, Jose, Huganir, Richard L., Malinow, Roberto·2006·Neuron
DOI 10.1016/j.neuron.2006.06.013
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Abstract

Incorporation of GluR1-containing AMPA receptors into synapses is essential to several forms of neural plasticity, including long-term potentiation (LTP). Numerous signaling pathways that trigger this process have been identified, but the direct modifications of GluR1 that control its incorporation into synapses are unclear. Here, we show that phosphorylation of GluR1 by PKC at a highly conserved serine 818 residue is increased during LTP and critical for LTP expression. GluR1 is phosphorylated by PKC at this site in vitro and in vivo. In addition, acute phosphorylation at GluR1 S818 by PKC, as well as a phosphomimetic mutation, promotes GluR1 synaptic incorporation. Conversely, preventing GluR1 S818 phosphorylation reduces LTP and blocks PKC-driven synaptic incorporation of GluR1. We conclude that the phosphorylation of GluR1 S818 by PKC is a critical event in the plasticity-driven synaptic incorporation of AMPA receptors.

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Crossref · 10.1016/j.neuron.2006.06.013

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  • During hippocampal LTP, PKC is activated to increase GluA1 S818 phosphorylation; peptide mimicking phospho-GluA1 S818 or shRNA-mediated knock-down of 4.1N both lead to decay of hippocampal LTP back to baseline, suggesting PKC/4.1N mediated increase in GluA1 exocytosis is necessary to maintain LTP.

    “During hippocampal LTP, PKC is activated to increase GluA1 S818 phosphorylation and a peptide mimicking phospho-GluA1 S818 or shRNA-mediated knock-down of 4.1N both lead to decay of hippocampal LTP back to baseline, suggesting that the PKC/4.1N mediated increase in GluA1 exocytosis is necessary to maintain LTP (Lin et al., 2009, Boehm et al., 2006).”

    From The AMPA Receptor Code of Synaptic Plasticity (2018) · cites this paper as Boehm et al., 2006

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Authors
Boehm, J., Kang, M.-G., Johnson, R. C., Esteban, J., Huganir, R. L., & Malinow, R.
Affiliations
  • Cold Spring Harbor Laboratory (US)
  • Howard Hughes Medical Institute (US)
  • University of Michigan (US)
Corresponding author
Malinow, Roberto
ORCID
Venue
Neuron
Publisher
Elsevier BV
Published
2006-07
Volume
51
Issue
2
Pages
213-225
ISSN
0896-6273 (ISSN-L)
DOI
10.1016/j.neuron.2006.06.013
OpenAlex
W2161036636
Cited by
382
References
8
Citations by year
2026: 6 · 2025: 16 · 2024: 12 · 2023: 5 · 2022: 9 · 2021: 11 · 2020: 13 · 2019: 8 · 2018: 18 · 2017: 20 · 2016: 19 · 2015: 20 · 2014: 27 · 2013: 36 · 2012: 23
FWCI
11.07
Type
journal article
Language
en
Open access
Licence
Locations
  • Neuron (publishedVersion)
  • PubMed (publishedVersion)
  • Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
  • DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
Funders
  • Alzheimer's Association
  • Deutsche Forschungsgemeinschaft
  • National Institutes of Health
  • Howard Hughes Medical Institute
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
AMPA receptors, GluR1, long-term potentiation, protein kinase C, synaptic plasticity, phosphomimetic mutations, receptor trafficking
MeSH terms
Animals, Binding Sites, Cell Line, Humans, Phosphorylation, Protein Kinase C, Synapses, Mutagenesis, Site-Directed, Long-Term Potentiation, Receptors, AMPA, Rats

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