Expression of NMDA receptor-dependent LTP in the hippocampus: bridging the divide
Open accessAbstract
A consensus has famously yet to emerge on the locus and mechanisms underlying the expression of the canonical NMDA receptor-dependent form of LTP. An objective assessment of the evidence leads us to conclude that both presynaptic and postsynaptic expression mechanisms contribute to this type of synaptic plasticity.
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The expression of NMDAR-dependent LTP is primarily postsynaptic, although a minor presynaptic component is difficult to entirely exclude.
“Although it is difficult to entirely exclude the possibility of a minor presynaptic component of NMDAR-dependent LTP, the evidence is overwhelming that its expression is primarily postsynaptic.”
From Synaptic memory and CaMKII (2023) · cites this paper as [31]
The Introduction says presynaptic mechanisms can play an important, even dominant, role in some experimental situations. The Discussion concludes that early LTP can be entirely presynaptic, entirely postsynaptic, or a combination of both. The paper therefore does not treat presynaptic expression as merely a minor possibility or postsynaptic expression as generally predominant. (LLM, conf=0.93)
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Experimental — accuracy not yet measuredgluN2B is a receptor essential to form LTP.
“Among them, miR-223, which targets the AMPA-selective glutamate receptor 2 (GluR2) and the NMDA glutamate receptor gluN2B [33] and miR-181a which regulates only gluN2B [66], a receptor essential to form LTP [8, 71].”
From Glia-to-neuron transfer of miRNAs via extracellular vesicles: a new mechanism underlying inflammation-induced synaptic alterations (2018) · cites this paper as [8]
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Cites
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“A similar conclusion was reached when Sr was used in place of Ca in the medium so that individual quanta could be resolved following synaptic stimulation [52].”
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- Authors
- Bliss, T. V., & Collingridge, G. L.
- Affiliations
- Seoul National University (KR)
- Corresponding author
- Bliss, Tim VP
- Collingridge, Graham L
- Venue
- Molecular Brain
- Published
- 2013
- Volume
- 6
- Issue
- 1
- Pages
- 5
- ISSN
- 1756-6606 (ISSN-L)
- PMC
- PMC3562207
- OpenAlex
- W2037352700
- Cited by
- 305
- References
- 12
- Citations by year
- 2026: 8 · 2025: 20 · 2024: 21 · 2023: 17 · 2022: 12 · 2021: 36 · 2020: 27 · 2019: 22 · 2018: 31 · 2017: 33 · 2016: 20 · 2015: 25 · 2014: 18 · 2013: 15
- FWCI
- 12.92
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Molecular Brain (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Bristol Research (University of Bristol) (submittedVersion)
- Funders
- Wellcome Trust (089703)
- Seoul National University
- Medical Research Council
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- NMDA receptor, long-term potentiation, hippocampus, synaptic plasticity, presynaptic plasticity, postsynaptic plasticity
- MeSH terms
- Animals, Hippocampus, Humans, Models, Biological, Synapses, Receptors, N-Methyl-D-Aspartate, Long-Term Potentiation
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