Long‐term plasticity in the hippocampus: maintaining within and ‘tagging’ between synapses
Abstract
Synapses between neurons are malleable biochemical structures, strengthening and diminishing over time dependent on the type of information they receive. This phenomenon known as synaptic plasticity underlies learning and memory, and its different forms, long‐term potentiation (LTP) and long‐term depression (LTD), perform varied cognitive roles in reinforcement, relearning and associating memories. Moreover, both LTP and LTD can exist in an early transient form (early‐LTP/LTD) or a late persistent form (late‐LTP/LTD), which are triggered by different induction protocols, and also differ in their dependence on protein synthesis and the involvement of key molecular players. Beyond homosynaptic modifications, synapses can also interact with one another. This is encapsulated in the synaptic tagging and capture hypothesis (STC), where synapses expressing early‐LTP/LTD present a ‘tag’ that can capture the protein synthesis products generated during a temporally proximal late‐LTP/LTD induction. This ‘tagging’ phenomenon forms the framework of synaptic interactions in various conditions and accounts for the cellular basis of the time‐dependent associativity of short‐lasting and long‐lasting memories. All these synaptic modifications take place under controlled neuronal conditions, regulated by subcellular elements such as epigenetic regulation, proteasomal degradation and neuromodulatory signals. Here, we review current understanding of the different forms of synaptic plasticity and its regulatory mechanisms in the hippocampus, a brain region critical for memory formation. We also discuss expression of plasticity in hippocampal CA2 area, a long‐overlooked narrow hippocampal subfield and the behavioural correlate of STC. Lastly, we put forth perspectives for an integrated view of memory representation in synapses.
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The nervous system needs a certain level of neuroplasticity to maintain normal cognitive and memory functions in the face of scattered neuronal dysfunction.
“To maintain normal cognitive and memory functions in the face of scattered neuronal dysfunction, the nervous system needs a certain level of neuroplasticity to allow for adjustments in circuitry through changes in synaptic strength and the formation of new synapses [171].”
From The extracellular matrix and perineuronal nets in memory (2022) · cites this paper as [171]
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The extracellular matrix and perineuronal nets in memory
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- Authors
- Bin Ibrahim, M. Z., Benoy, A., & Sajikumar, S.
- Affiliations
- Department of Physiology Yong Loo Lin School of Medicine National University of Singapore Singapore
- National University of Singapore (SG)
- Corresponding author
- Sajikumar, Sreedharan
- Venue
- The FEBS Journal
- Publisher
- Wiley
- Published
- 2021-06-25
- Volume
- 289
- Issue
- 8
- Pages
- 2176-2201
- ISSN
- 1742-464X (ISSN-L)
- 1742-4658
- OpenAlex
- W3169879005
- Cited by
- 137
- References
- 21
- Citations by year
- 2026: 27 · 2025: 33 · 2024: 33 · 2023: 22 · 2022: 20 · 2021: 1
- FWCI
- 2.91
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- FEBS Journal (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National University of Singapore
- National Medical Research Council (NMRC‐OFIRG‐0037‐2017)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- synaptic plasticity, hippocampus, long-term potentiation, long-term depression, protein synthesis, memory consolidation, epigenetic regulation, proteasomal degradation, neuromodulation, memory representation
- MeSH terms
- Hippocampus, Neuronal Plasticity, Synapses, Long-Term Potentiation, Epigenesis, Genetic
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