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Specific Roles of AMPA Receptor Subunit GluR1 (GluA1) Phosphorylation Sites in Regulating Synaptic Plasticity in the CA1 Region of Hippocampus
Open accessAbstract
Activity-dependent changes in excitatory synaptic transmission in the CNS have been shown to depend on the regulation of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPARs). In particular, several lines of evidence suggest that reversible phosphorylation of AMPAR subunit glutamate receptor 1 (GluR1, also referred to as GluA1 or GluR-A) plays a role in long-term potentiation (LTP) and long-term depression (LTD). We previously reported that regulation of serines (S) 831 and 845 on the GluR1 subunit may play a critical role in bidirectional synaptic plasticity in the Schaffer collateral inputs to CA1. Specifically, gene knockin mice lacking both S831 and S845 phosphorylation sites ("double phosphomutants"), where both serine residues were replaced by alanines (A), showed a faster decaying LTP and a deficit in LTD. To determine which of the two phosphorylation sites was responsible for the phenotype, we have now generated two lines of gene knockin mice: one that specifically lacks S831 (S831A mutants) and another that lacks only S845 (S845A mutants). We found that S831A mutants display normal LTP and LTD, whereas S845A mutants show a specific deficit in LTD. Taken together with our previous results from the "double phosphomutants," our data suggest that either S831 or S845 alone may support LTP, whereas the S845 site is critical for LTD expression.
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In the citing paper
“GluA1 S845/831A and S845A knock-in mice are deficient in LTD, but S831A mice express normal LTD, further indicating that LTD requires regulation of only S845 phosphorylation”
From AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors (2012) · cites this paper as Lee et al., 2010
In the citing paper
“dephosphorylation and endocytosis of this pool of GluA1 is required for LTD, explaining why S845A knock-in mice that lack this receptor pool are deficient in LTD”
From AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors (2012) · cites this paper as Lee et al., 2010
In the citing paper
“LTD is impaired in GluA1-S845A knock-in mice (Lee et al., 2010), where it was found that S845 phosphorylation stabilizes GluA1 homomers in extrasynaptic locations where they exchange in and out of the synapse but are removed by LTD”
From AKAP150-Anchored Calcineurin Regulates Synaptic Plasticity by Limiting Synaptic Incorporation of Ca2+-Permeable AMPA Receptors (2012) · cites this paper as Lee et al., 2010
In the citing paper
“A further issue is that replacement by alanine of either one of these residues does not affect LTP (271)”
From Synaptic memory and CaMKII (2023) · cites this paper as [271]
In the citing paper
“GluA1 S845 dephosphorylation is critical for hippocampal LTD, as the GluA1 S845A mutation results in impaired LTD (Lee et al., 2003, Lee et al., 2010), indicating that the induction of LTD requires PKA phosphorylation of GluA1 even though receptors are eventually dephosphorylated (Huganir and Nicoll, 2013).”
From The AMPA Receptor Code of Synaptic Plasticity (2018) · cites this paper as Lee et al., 2010
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Metadata
- Authors
- Lee, H.-K., Takamiya, K., He, K., Song, L., & Huganir, R. L.
- Affiliations
- Howard Hughes Medical Institute (US)
- University of Maryland, College Park (US)
- Corresponding author
- Huganir, Richard L.
- Venue
- Journal of Neurophysiology
- Publisher
- American Physiological Society
- Published
- 2010-01
- Volume
- 103
- Issue
- 1
- Pages
- 479-489
- ISSN
- 0022-3077 (ISSN-L)
- 1522-1598
- PMC
- PMC2807233
- OpenAlex
- W2162552344
- Cited by
- 261
- References
- 65
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 13 · 2023: 13 · 2022: 17 · 2021: 14 · 2020: 18 · 2019: 17 · 2018: 18 · 2017: 11 · 2016: 24 · 2015: 22 · 2014: 19 · 2013: 23 · 2012: 13
- FWCI
- 5.13
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Neurophysiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- National Eye Institute (R01EY014882)
- National Institute of Neurological Disorders and Stroke (R01NS036715)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Keywords
- GluR1, AMPA receptors, GluR1 phosphorylation, long-term potentiation, long-term depression, bidirectional synaptic plasticity, hippocampal CA1, Schaffer collaterals, excitatory synaptic transmission
- MeSH terms
- Aging, Amino Acid Sequence, Animals, Base Sequence, Male, Mice, Inbred C57BL, Mice, Transgenic, Molecular Sequence Data, Mutation, Synaptic Transmission, Neurons, Phosphorylation, Synapses, Long-Term Potentiation, Receptors, AMPA, Long-Term Synaptic Depression, Mice, Gene Knock-In Techniques, CA1 Region, Hippocampal, In Vitro Techniques
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