Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (595 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A persistent increase in synaptic efficacy, usually induced by appropriate activation of the same synapses. The phenomenological properties of long-term potentiation suggest that it may be a cellular mechanism of learning and memory.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Long Term Potentiation; Long-Term Potentiations; Potentiation, Long-Term; Potentiations, Long-Term.
Where it fits in the MeSH classification
- Broader topics
- Neuronal Plasticity
Research landscape
PubMed indexes 11,402 records tagged with the MeSH heading “Long-Term Potentiation” (counts retrieved 2026-10-29). 1,579 of them (13.8%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 3,976 records.
Reviews account for 1,285 records (11.3%) and meta-analyses for 2. Randomized controlled trials number 52 (0.5%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,921 |
| 2000-2009 | 3,926 |
| 2010-2019 | 3,976 |
| 2020 onward | 1,579 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,285 | 11.3% |
| Meta-analyses | 2 | 0.0% |
| Randomized controlled trials | 52 | 0.5% |
Method: PubMed query "Long-Term Potentiation"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in neuroscience
Neuroscience draws on tools with different strengths: cellular and animal work can manipulate circuits directly, while human imaging and electrophysiology observe the living brain at lower resolution. Small imaging studies are prone to false positives, and findings in animals do not always carry over to people. Clinical neurology and psychiatry rely on trials and cohort studies whose outcomes are often symptom scales. Check the species, the sample size, how the outcome was measured and whether results were replicated.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| LTP Induction Boosts Glutamate Spillover by Driving Withdrawal of Perisynaptic Astroglia | 2020 | Research article Design not recorded in structured metadata | 223 | cc by PMID 32976770 · DOI · PMC7736499 |
| Stress gates an astrocytic energy reservoir to impair synaptic plasticity | 2020 | Research article Design not recorded in structured metadata | 132 | cc by PMID 32332733 · DOI · PMC7181611 |
| Rapid active zone remodeling consolidates presynaptic potentiation | 2019 | Research article Design not recorded in structured metadata | 127 | cc by PMID 30842428 · DOI · PMC6403334 |
| D1/D5 receptor activation promotes long-term potentiation and synaptic tagging/capture in hippocampal area CA2 | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 40983366 · DOI · PMC12871914 |
LTP Induction Boosts Glutamate Spillover by Driving Withdrawal of Perisynaptic Astroglia [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Extrasynaptic actions of glutamate are limited by high-affinity transporters expressed by perisynaptic astroglial processes (PAPs): this helps maintain point-to-point transmission in excitatory circuits.
- Closing excerpt
- We have therefore uncovered a mechanism by which a memory trace at one synapse could alter signal handling by multiple neighboring connections.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (148 words)
Extrasynaptic actions of glutamate are limited by high-affinity transporters expressed by perisynaptic astroglial processes (PAPs): this helps maintain point-to-point transmission in excitatory circuits. Memory formation in the brain is associated with synaptic remodeling, but how this affects PAPs and therefore extrasynaptic glutamate actions is poorly understood. Here, we used advanced imaging methods, in situ and in vivo, to find that a classical synaptic memory mechanism, long-term potentiation (LTP), triggers withdrawal of PAPs from potentiated synapses. Optical glutamate sensors combined with patch-clamp and 3D molecular localization reveal that LTP induction thus prompts spatial retreat of astroglial glutamate transporters, boosting glutamate spillover and NMDA-receptor-mediated inter-synaptic cross-talk. The LTP-triggered PAP withdrawal involves NKCC1 transporters and the actin-controlling protein cofilin but does not depend on major Ca2+-dependent cascades in astrocytes. We have therefore uncovered a mechanism by which a memory trace at one synapse could alter signal handling by multiple neighboring connections.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32976770 · DOI · PMC7736499
Stress gates an astrocytic energy reservoir to impair synaptic plasticity [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Astrocytes support the energy demands of synaptic transmission and plasticity.
- Closing excerpt
- This gating of synaptic plasticity in stress by astrocytic metabolic networks indicates a broader role of astrocyte bioenergetics in determining how experience-dependent information is controlled.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
Astrocytes support the energy demands of synaptic transmission and plasticity. Enduring changes in synaptic efficacy are highly sensitive to stress, yet whether changes to astrocyte bioenergetic control of synapses contributes to stress-impaired plasticity is unclear. Here we show in mice that stress constrains the shuttling of glucose and lactate through astrocyte networks, creating a barrier for neuronal access to an astrocytic energy reservoir in the hippocampus and neocortex, compromising long-term potentiation. Impairing astrocytic delivery of energy substrates by reducing astrocyte gap junction coupling with dominant negative connexin 43 or by disrupting lactate efflux was sufficient to mimic the effects of stress on long-term potentiation. Furthermore, direct restoration of the astrocyte lactate supply alone rescued stress-impaired synaptic plasticity, which was blocked by inhibiting neural lactate uptake. This gating of synaptic plasticity in stress by astrocytic metabolic networks indicates a broader role of astrocyte bioenergetics in determining how experience-dependent information is controlled.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32332733 · DOI · PMC7181611
Rapid active zone remodeling consolidates presynaptic potentiation [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Neuronal communication across synapses relies on neurotransmitter release from presynaptic active zones (AZs) followed by postsynaptic transmitter detection.
- Closing excerpt
- Together, while immediate synaptic potentiation capitalizes on available material, it triggers the coincident incorporation of modular release sites to consolidate synaptic potentiation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
Neuronal communication across synapses relies on neurotransmitter release from presynaptic active zones (AZs) followed by postsynaptic transmitter detection. Synaptic plasticity homeostatically maintains functionality during perturbations and enables memory formation. Postsynaptic plasticity targets neurotransmitter receptors, but presynaptic mechanisms regulating the neurotransmitter release apparatus remain largely enigmatic. By studying Drosophila neuromuscular junctions (NMJs) we show that AZs consist of nano-modular release sites and identify a molecular sequence that adds modules within minutes of inducing homeostatic plasticity. This requires cognate transport machinery and specific AZ-scaffolding proteins. Structural remodeling is not required for immediate potentiation of neurotransmitter release, but necessary to sustain potentiation over longer timescales. Finally, mutations in Unc13 disrupting homeostatic plasticity at the NMJ also impair short-term memory when central neurons are targeted, suggesting that both plasticity mechanisms utilize Unc13. Together, while immediate synaptic potentiation capitalizes on available material, it triggers the coincident incorporation of modular release sites to consolidate synaptic potentiation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30842428 · DOI · PMC6403334
D1/D5 receptor activation promotes long-term potentiation and synaptic tagging/capture in hippocampal area CA2 [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Hippocampal area CA2 plays an important role in social memory formation.
- Closing excerpt
- Thus, we propose a link between neuropsychiatric diseases related to impaired dopamine transmission and deficits in hippocampus-dependent social memory.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (147 words)
Hippocampal area CA2 plays an important role in social memory formation. However, CA2 is characterised by plasticity-resistant Schaffer Collateral-CA2 (SC-CA2) synapses and highly plastic entorhinal cortex-CA2 (EC-CA2) synapses. Despite abundant dopaminergic input, the relationship between dopamine signalling and area CA2 synaptic plasticity remains unexplored. Here, we show that SKF-38393-mediated dopamine D1-like receptor (dopamine D1 and D5 receptors (D1R and D5R)) activation differentially primes CA2 inputs in an N-methyl-D-aspartate receptor (NMDAR)- and protein synthesis-dependent manner. We defined an inverted U-shape relationship between SKF-38393 concentration and EC-CA2 potentiation. Additionally, we observed a priming effect on SC-CA2 plasticity with 50 μm SKF-38393, relieving plasticity resistance. We also demonstrated that this effect follows canonical protein kinase A (PKA) signalling. Collectively, our results show that D1R activation primes the CA2 for synaptic plasticity. Thus, we propose a link between neuropsychiatric diseases related to impaired dopamine transmission and deficits in hippocampus-dependent social memory.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40983366 · DOI · PMC12871914
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article LTP and LTD: an embarrassment of riches [5]
- Research article Long-term potentiation--a decade of progress? [6]
- Research article Long-term potentiation and memory [7]
- Research article Synaptic plasticity: taming the beast [8]
- Research article Central sensitization and LTP: do pain and memory share similar mechanisms? [9]
- Research article Mechanisms of CaMKII action in long-term potentiation [10]
References
- Henneberger C, Bard L, Panatier A, Reynolds JP, Kopach O, Medvedev NI, et al.. LTP Induction Boosts Glutamate Spillover by Driving Withdrawal of Perisynaptic Astroglia. . 2020. PMID 32976770 · DOI · PMC7736499
- Murphy-Royal C, Johnston AD, Boyce AKJ, Diaz-Castro B, Institoris A, Peringod G, et al.. Stress gates an astrocytic energy reservoir to impair synaptic plasticity. . 2020. PMID 32332733 · DOI · PMC7181611
- Böhme MA, McCarthy AW, Grasskamp AT, Beuschel CB, Goel P, Jusyte M, et al.. Rapid active zone remodeling consolidates presynaptic potentiation. . 2019. PMID 30842428 · DOI · PMC6403334
- Chua K, Chong YS, Sajikumar S. D1/D5 receptor activation promotes long-term potentiation and synaptic tagging/capture in hippocampal area CA2. . 2026. PMID 40983366 · DOI · PMC12871914
- Malenka RC, Bear MF. LTP and LTD: an embarrassment of riches. Neuron. 2004. PMID 15450156 · DOI
- Malenka RC, Nicoll RA. Long-term potentiation--a decade of progress?. Science. 1999. PMID 10489359 · DOI
- Lynch MA. Long-term potentiation and memory. Physiol Rev. 2004. PMID 14715912 · DOI
- Abbott LF, Nelson SB. Synaptic plasticity: taming the beast. Nat Neurosci. 2000. PMID 11127835 · DOI
- Ji RR, Kohno T, Moore KA, Woolf CJ. Central sensitization and LTP: do pain and memory share similar mechanisms?. Trends Neurosci. 2003. PMID 14624855 · DOI
- Lisman J, Yasuda R, Raghavachari S. Mechanisms of CaMKII action in long-term potentiation. Nat Rev Neurosci. 2012. PMID 22334212 · DOI · PMC4050655
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.