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 (593 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
The communication from a neuron to a target (neuron, muscle, or secretory cell) across a synapse. In chemical synaptic transmission, the presynaptic neuron releases a neurotransmitter that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across electrical synapses.
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: Transmission, Neural; Neural Transmission; Transmission, Synaptic; Neurotransmission.
Where it fits in the MeSH classification
- Broader topics
- Signal Transduction; Electrophysiological Phenomena; Nervous System Physiological Phenomena
- Narrower topics
- Postsynaptic Potential Summation; Synaptic Potentials
- See also
- Synapses; Gap Junctions
Related concepts
- Neurons
- Synapse
- Neurotransmitter
- Electrical Synapses
Research landscape
PubMed indexes 69,380 records tagged with the MeSH heading “Synaptic Transmission” (counts retrieved 2026-10-29). 5,121 of them (7.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 28,068 records.
Reviews account for 9,254 records (13.3%) and meta-analyses for 25. Randomized controlled trials number 244 (0.4%) 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 | 28,068 |
| 2000-2009 | 19,645 |
| 2010-2019 | 16,546 |
| 2020 onward | 5,121 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 9,254 | 13.3% |
| Meta-analyses | 25 | 0.0% |
| Randomized controlled trials | 244 | 0.4% |
Method: PubMed query "Synaptic Transmission"[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 |
|---|---|---|---|---|
| Glutamate indicators with improved activation kinetics and localization for imaging synaptic transmission | 2023 | Research article Design not recorded in structured metadata | 173 | cc by PMID 37142767 · DOI · PMC10250197 |
| Cholesterol imbalance and neurotransmission defects in neurodegeneration | 2024 | Review article Design not recorded in structured metadata | 75 | cc by PMID 39085348 · DOI · PMC11371908 |
| Neurotransmitters Regulation and Food Intake: The Role of Dietary Sources in Neurotransmission | 2022 | Review article Design not recorded in structured metadata | 54 | cc by PMID 36615404 · DOI · PMC9822089 |
| Glutamate indicators with increased sensitivity and tailored deactivation rates | 2026 | Research article Design not recorded in structured metadata | 13 | cc by PMID 41436654 · DOI · PMC12904790 |
Glutamate indicators with improved activation kinetics and localization for imaging synaptic transmission [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The fluorescent glutamate indicator iGluSnFR enables imaging of neurotransmission with genetic and molecular specificity.
- Closing excerpt
- In vibrissal sensory cortex layer 4, we used iGluSnFR3 to characterize distinct patterns of touch-evoked feedforward input from thalamocortical boutons and both feedforward and recurrent input onto L4 cortical neuron dendritic spines.
- 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 (144 words)
The fluorescent glutamate indicator iGluSnFR enables imaging of neurotransmission with genetic and molecular specificity. However, existing iGluSnFR variants exhibit low in vivo signal-to-noise ratios, saturating activation kinetics and exclusion from postsynaptic densities. Using a multiassay screen in bacteria, soluble protein and cultured neurons, we generated variants with improved signal-to-noise ratios and kinetics. We developed surface display constructs that improve iGluSnFR's nanoscopic localization to postsynapses. The resulting indicator iGluSnFR3 exhibits rapid nonsaturating activation kinetics and reports synaptic glutamate release with decreased saturation and increased specificity versus extrasynaptic signals in cultured neurons. Simultaneous imaging and electrophysiology at individual boutons in mouse visual cortex showed that iGluSnFR3 transients report single action potentials with high specificity. In vibrissal sensory cortex layer 4, we used iGluSnFR3 to characterize distinct patterns of touch-evoked feedforward input from thalamocortical boutons and both feedforward and recurrent input onto L4 cortical neuron dendritic spines.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37142767 · DOI · PMC10250197
Cholesterol imbalance and neurotransmission defects in neurodegeneration [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The brain contains the highest concentration of cholesterol in the human body, which emphasizes the importance of cholesterol in brain physiology.
- Closing excerpt
- This review aims to explore the molecular and pathological mechanisms by which cholesterol imbalance can lead to neurotransmission defects and neurodegeneration, focusing on four key mechanisms: (1) synaptic dysfunction, (2) alterations in membrane structure and protein clustering, (3) oligomers of amyloid beta (Aβ) protein, and (4) α-synuclein aggregation.
- 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 (131 words)
The brain contains the highest concentration of cholesterol in the human body, which emphasizes the importance of cholesterol in brain physiology. Cholesterol is involved in neurogenesis and synaptogenesis, and age-related reductions in cholesterol levels can lead to synaptic loss and impaired synaptic plasticity, which potentially contribute to neurodegeneration. The maintenance of cholesterol homeostasis in the neuronal plasma membrane is essential for normal brain function, and imbalances in cholesterol distribution are associated with various neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. This review aims to explore the molecular and pathological mechanisms by which cholesterol imbalance can lead to neurotransmission defects and neurodegeneration, focusing on four key mechanisms: (1) synaptic dysfunction, (2) alterations in membrane structure and protein clustering, (3) oligomers of amyloid beta (Aβ) protein, and (4) α-synuclein aggregation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39085348 · DOI · PMC11371908
Neurotransmitters Regulation and Food Intake: The Role of Dietary Sources in Neurotransmission [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Neurotransmitters (NTs) are biologically active chemicals, which mediate the electrochemical transmission between neurons.
- Closing excerpt
- Interventional strategies supported by evidence should be encouraged.
- 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 (175 words)
Neurotransmitters (NTs) are biologically active chemicals, which mediate the electrochemical transmission between neurons. NTs control numerous organic functions particularly crucial for life, including movement, emotional responses, and the physical ability to feel pleasure and pain. These molecules are synthesized from simple, very common precursors. Many types of NTs have both excitatory and inhibitory effects. Neurotransmitters' imbalance can cause many diseases and disorders, such as Parkinson's disease, depression, insomnia, increased anxiety, memory loss, etc. Natural food sources containing NTs and/or their precursors would be a potential option to help maintain the balance of NTs to prevent brain and psychiatric disorders. The level of NTs could be influenced, therefore, by targeting dietary habits and nutritional regimens. The progressive implementation of nutritional approaches in clinical practice has made it necessary to infer more about some of the nutritional NTs in neuropsychiatry. However, the importance of the intake of nutritional NTs requires further understanding, since there are no prior significant studies about their bioavailability, clinical significance, and effects on nerve cells. Interventional strategies supported by evidence should be encouraged.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36615404 · DOI · PMC9822089
Glutamate indicators with increased sensitivity and tailored deactivation rates [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Understanding how neurons integrate signals from thousands of input synapses requires methods to monitor neurotransmission across many sites simultaneously.
- Closing excerpt
- The iGluSnFR4 variants extend the speed, sensitivity and scalability of glutamate imaging, enabling direct observation of information flow through neural networks in the intact brain.
- 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 (143 words)
Understanding how neurons integrate signals from thousands of input synapses requires methods to monitor neurotransmission across many sites simultaneously. The fluorescent protein glutamate indicator iGluSnFR enables visualization of synaptic signaling, but the sensitivity, scale and speed of such measurements are limited by existing variants. Here we developed two highly sensitive fourth-generation iGluSnFR variants with fast activation and tailored deactivation rates: iGluSnFR4f for tracking rapid dynamics, and iGluSnFR4s for recording from large populations of synapses. These indicators detect glutamate with high spatial specificity and single-vesicle sensitivity in vivo. We used them to record natural patterns of synaptic transmission across multiple experimental contexts in mice, including two-photon imaging in cortical layers 1-4 and hippocampal CA1, and photometry in the midbrain. The iGluSnFR4 variants extend the speed, sensitivity and scalability of glutamate imaging, enabling direct observation of information flow through neural networks in the intact brain.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41436654 · DOI · PMC12904790
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 Hippocampal GABAergic Inhibitory Interneurons [5]
- Research article Brain Glucose Metabolism: Integration of Energetics with Function [6]
- Research article Synaptic Plasticity Forms and Functions [7]
- Research article Mitochondria at the neuronal presynapse in health and disease [8]
- Research article BDNF signaling in context: From synaptic regulation to psychiatric disorders [9]
- Research article Taste buds: cells, signals and synapses [10]
References
- Aggarwal A, Liu R, Chen Y, Ralowicz AJ, Bergerson SJ, Tomaska F, et al.. Glutamate indicators with improved activation kinetics and localization for imaging synaptic transmission. . 2023. PMID 37142767 · DOI · PMC10250197
- Shin KC, Ali Moussa HY, Park Y. Cholesterol imbalance and neurotransmission defects in neurodegeneration. . 2024. PMID 39085348 · DOI · PMC11371908
- Gasmi A, Nasreen A, Menzel A, Gasmi Benahmed A, Pivina L, Noor S, et al.. Neurotransmitters Regulation and Food Intake: The Role of Dietary Sources in Neurotransmission. . 2022. PMID 36615404 · DOI · PMC9822089
- Aggarwal A, Negrean A, Chen Y, Iyer R, Reep D, Liu A, et al.. Glutamate indicators with increased sensitivity and tailored deactivation rates. . 2026. PMID 41436654 · DOI · PMC12904790
- Pelkey KA, Chittajallu R, Craig MT, Tricoire L, Wester JC, McBain CJ. Hippocampal GABAergic Inhibitory Interneurons. Physiol Rev. 2017. PMID 28954853 · DOI · PMC6151493
- Dienel GA. Brain Glucose Metabolism: Integration of Energetics with Function. Physiol Rev. 2019. PMID 30565508 · DOI
- Magee JC, Grienberger C. Synaptic Plasticity Forms and Functions. Annu Rev Neurosci. 2020. PMID 32075520 · DOI
- Devine MJ, Kittler JT. Mitochondria at the neuronal presynapse in health and disease. Nat Rev Neurosci. 2018. PMID 29348666 · DOI
- Wang CS, Kavalali ET, Monteggia LM. BDNF signaling in context: From synaptic regulation to psychiatric disorders. Cell. 2022. PMID 34963057 · DOI · PMC8741740
- Roper SD, Chaudhari N. Taste buds: cells, signals and synapses. Nat Rev Neurosci. 2017. PMID 28655883 · DOI · PMC5958546
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.