The DOI matches its Crossref record; 166 of the 166 references it cites were found in a registry or an index.
Translational Control in Synaptic Plasticity and Cognitive Dysfunction
Open accessAbstract
Activity-dependent changes in the strength of synaptic connections are fundamental to the formation and maintenance of memory. The mechanisms underlying persistent changes in synaptic strength in the hippocampus, specifically long-term potentiation and depression, depend on new protein synthesis. Such changes are thought to be orchestrated by engaging the signaling pathways that regulate mRNA translation in neurons. In this review, we discuss the key regulatory pathways that govern translational control in response to synaptic activity and the mRNA populations that are specifically targeted by these pathways. The critical contribution of regulatory control over new protein synthesis to proper cognitive function is underscored by human disorders associated with either silencing or mutation of genes encoding proteins that directly regulate translation. In light of these clinical implications, we also consider the therapeutic potential of targeting dysregulated translational control to treat cognitive disorders of synaptic dysfunction.
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“When NMDAR activity is reduced, as with ketamine or (2R,6R)-hydroxynorketamine (2R,6R-HNK), eEF2K activity falls, eEF2 becomes dephosphorylated, and translational inhibition is rapidly lifted [141,143,145].”
From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [143]
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“Translational control is a central driver of rapid synaptic plasticity, with eEF2K acting as a molecular brake on protein synthesis [141,142,143].”
From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [143]
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“Neuronal protein synthesis has been well established as crucial for synaptic function and memory formation, and it is dysregulated in Alzheimer’s (43).”
From Apolipoprotein E2 Stimulates Protein Synthesis and Promotes Melanoma Progression and Metastasis (2023) · cites this paper as [43]
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“The synthesis of new proteins is necessary for long-term changes in synaptic plasticity and learning (132–134). In this context, learning and long-term memory formation are improved by enhanced histone acetylation (135), which could be improved by HDAC inhibitors (HDACi).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [134]
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Citations
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Metadata
- Authors
- Buffington, S. A., Huang, W., & Costa-Mattioli, M.
- Affiliations
- Baylor College of Medicine (US)
- Department of Neuroscience, Memory and Brain Research Center, Baylor College of Medicine, Houston, Texas 77030;, ,
- Venue
- Annual Review of Neuroscience
- Publisher
- Annual Reviews
- Published
- 2014-07-08
- Volume
- 37
- Issue
- 1
- Pages
- 17-38
- ISSN
- 0147-006X (ISSN-L)
- 1545-4126
- PMC
- PMC4721605
- OpenAlex
- W2120053143
- Cited by
- 348
- References
- 166
- Citations by year
- 2026: 17 · 2025: 23 · 2024: 21 · 2023: 20 · 2022: 24 · 2021: 36 · 2020: 36 · 2019: 30 · 2018: 43 · 2017: 33 · 2016: 33 · 2015: 21 · 2014: 11
- FWCI
- 3.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annual Review of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Defense
- Searle Scholars Program
- National Institute of Mental Health
- National Institute of Neurological Disorders and Stroke (R01NS076708)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA and protein synthesis mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- translational regulation, synaptic plasticity, long-term potentiation, long-term depression, hippocampus, mRNA translation, memory formation, cognitive impairment, synaptic dysfunction
- MeSH terms
- Animals, Cognition Disorders, Hippocampus, Humans, Models, Biological, Nerve Tissue Proteins, Neuronal Plasticity, Protein Biosynthesis, Signal Transduction
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