Synaptic AMPA receptor plasticity and behavior
Open accessAbstract
The ability to change behavior likely depends on the selective strengthening and weakening of brain synapses. The cellular models of synaptic plasticity, long-term potentiation (LTP) and depression (LTD) of synaptic strength, can be expressed by the synaptic insertion or removal of AMPA receptors (AMPARs), respectively. We here present an overview of studies that have used animal models to show that such AMPAR trafficking underlies several experience-driven phenomena-from neuronal circuit formation to the modification of behavior. We argue that monitoring and manipulating synaptic AMPAR trafficking represents an attractive means to study cognitive function and dysfunction in animal models.
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The post-synaptic density contains 'slots' that might be occupied by AMPARs supplied by lateral diffusion from the peri-synaptic region.
“A prominent model of synaptic strength posits that the post-synaptic density (PSD), a dense network of synaptic scaffolding, adhesion and cytoskeletal proteins, contains ‘slots’ that might be occupied by AMPARs supplied by lateral diffusion from the peri-synaptic region (Opazo et al., 2012, Huganir and Nicoll, 2013, Kessels and Malinow, 2009).”
From The AMPA Receptor Code of Synaptic Plasticity (2018) · cites this paper as Kessels and Malinow, 2009
In “Synaptic Strengthening by AMPAR Trafficking” (page unavailable), the paper describes a synaptic AMPAR ‘slot’ formed by interacting proteins. “Synaptic Trafficking in the Absence of Plasticity” describes receptor exchange from extrasynaptic to synaptic sites. Neither passage specifies lateral diffusion from the perisynaptic region into PSD slots, so that mechanism is not supported by this source. (LLM, conf=0.84)
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- Authors
- Kessels, H. W., & Malinow, R.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Kessels, Helmut W.
- Malinow, Roberto
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2009-02
- Volume
- 61
- Issue
- 3
- Pages
- 340-350
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC3917551
- OpenAlex
- W2059117412
- Cited by
- 993
- References
- 21
- Citations by year
- 2026: 23 · 2025: 32 · 2024: 33 · 2023: 31 · 2022: 37 · 2021: 62 · 2020: 53 · 2019: 54 · 2018: 57 · 2017: 53 · 2016: 45 · 2015: 75 · 2014: 79 · 2013: 78 · 2012: 85
- FWCI
- 8.12
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (AG032132, R01AG032132)
- National Institute of Mental Health (R01MH049159, R37MH049159, MH049159)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- AMPA receptors, synaptic plasticity, long-term potentiation, long-term depression, receptor trafficking, behavior modification, cognitive impairment, animal models of behavior
- MeSH terms
- Animals, Behavior, Brain, Cognition, Humans, Learning, Synaptic Transmission, Neuronal Plasticity, Synapses, Receptors, AMPA, Protein Transport
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