Synaptic Signaling in Learning and Memory
Open accessAbstract
Learning and memory require the formation of new neural networks in the brain. A key mechanism underlying this process is synaptic plasticity at excitatory synapses, which connect neurons into networks. Excitatory synaptic transmission happens when glutamate, the excitatory neurotransmitter, activates receptors on the postsynaptic neuron. Synaptic plasticity is a higher-level process in which the strength of excitatory synapses is altered in response to the pattern of activity at the synapse. It is initiated in the postsynaptic compartment, where the precise pattern of influx of calcium through activated glutamate receptors leads either to the addition of new receptors and enlargement of the synapse (long-term potentiation) or the removal of receptors and shrinkage of the synapse (long-term depression). Calcium/calmodulin-regulated enzymes and small GTPases collaborate to control this highly tuned mechanism.
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For early plasticity to last, downstream signaling must stabilize structure, transcription, and protein synthesis.
“For early plasticity to last, downstream signaling must stabilize structure, transcription, and protein synthesis [34,41].”
From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [34]
The Introduction (page not provided) describes early structural changes followed by signaling that increases local protein synthesis and activates transcription; it says these later changes can affect neuronal structure for hours to a lifetime. It does not establish that all three processes must be stabilized for early plasticity to last, so the claim overstates their necessity. (LLM, conf=0.82)
Experimental — accuracy not yet measuredSynaptic plasticity comprises two interdependent phases: induction, in which patterns of neuronal activity rapidly alter synaptic efficacy, and consolidation, in which these initially labile changes are stabilized to support persistent circuit reorganization.
“Synaptic plasticity comprises two interdependent phases: induction, in which patterns of neuronal activity rapidly alter synaptic efficacy, and consolidation, in which these initially labile changes are stabilized to support persistent circuit reorganization [34,35].”
From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [34]
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- Authors
- Kennedy, M. B.
- Affiliations
- California Institute of Technology (US)
- Corresponding author
- Kennedy, Mary B.
- ORCID
- Kennedy, Mary B.
- Venue
- Cold Spring Harbor Perspectives in Biology
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2013-12-30
- Volume
- 8
- Issue
- 2
- Pages
- a016824
- ISSN
- 1943-0264 (ISSN-L)
- PMC
- PMC4743082
- OpenAlex
- W2166158223
- Cited by
- 270
- References
- 137
- Citations by year
- 2026: 30 · 2025: 66 · 2024: 39 · 2023: 28 · 2022: 23 · 2021: 29 · 2020: 19 · 2019: 10 · 2018: 8 · 2017: 6 · 2016: 9 · 2015: 1 · 2014: 1 · 2013: 1
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Perspectives in Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion, cc-by-nc)
- Funders
- National Institute of Mental Health (R01MH095095)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- synaptic plasticity, learning and memory, excitatory synapses, glutamate receptors, long-term potentiation, long-term depression, calcium signaling, calmodulin, small GTPases, postsynaptic compartment, neural network formation
- MeSH terms
- Animals, Humans, Memory, Synaptic Transmission, Neuronal Plasticity, Receptors, AMPA, Neurotransmitter Agents, GTP Phosphohydrolases
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