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 (657 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
Branch-like terminations of nerve fibers, sensory or motor neurons. Endings of sensory neurons are the beginnings of afferent pathway to the central nervous system. Endings of motor neurons are the terminals of axons at the muscle cells. Nerve endings which release neurotransmitters are called presynaptic terminals.
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: Ending, Nerve; Endings, Nerve; Nerve Ending.
Where it fits in the MeSH classification
- Broader topics
- Peripheral Nervous System
- Narrower topics
- Neuroeffector Junction
- See also
- Presynaptic Terminals
Related concepts
- Nerve Fibers
- Neurons
- Central Nervous System
- Presynaptic Terminals
Research landscape
PubMed indexes 33,253 records tagged with the MeSH heading “Nerve Endings” (counts retrieved 2026-10-29). 1,360 of them (4.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 24,662 records.
Reviews account for 2,885 records (8.7%) and meta-analyses for 9. Randomized controlled trials number 492 (1.5%) 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 | 24,662 |
| 2000-2009 | 4,005 |
| 2010-2019 | 3,226 |
| 2020 onward | 1,360 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,885 | 8.7% |
| Meta-analyses | 9 | 0.0% |
| Randomized controlled trials | 492 | 1.5% |
Method: PubMed query "Nerve Endings"[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 |
|---|---|---|---|---|
| The neuromuscular junction is a focal point of mTORC1 signaling in sarcopenia | 2020 | Research article Design not recorded in structured metadata | 173 | cc by PMID 32908143 · DOI · PMC7481251 |
| Sensory innervation in porous endplates by Netrin-1 from osteoclasts mediates PGE2-induced spinal hypersensitivity in mice | 2019 | Research article Design not recorded in structured metadata | 137 | cc by PMID 31822662 · DOI · PMC6904550 |
| Axonal TDP-43 condensates drive neuromuscular junction disruption through inhibition of local synthesis of nuclear encoded mitochondrial proteins | 2021 | Research article Design not recorded in structured metadata | 130 | cc by PMID 34824257 · DOI · PMC8617040 |
| Age-Associated Dysregulation of Postsynaptic Mitochondria Perturbs Reinnervation Kinetics | 2026 | Research article Design not recorded in structured metadata | 9 | cc by PMID 41496579 · DOI · PMC12775679 |
The neuromuscular junction is a focal point of mTORC1 signaling in sarcopenia [1]
Abstract reading summary — source excerpts
- Opening excerpt
- With human median lifespan extending into the 80s in many developed countries, the societal burden of age-related muscle loss (sarcopenia) is increasing.
- Closing excerpt
- We uncover inter-muscle divergence in the primary drivers of sarcopenia and identify the neuromuscular junction as a focal point of mTORC1-driven muscle aging.
- 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)
With human median lifespan extending into the 80s in many developed countries, the societal burden of age-related muscle loss (sarcopenia) is increasing. mTORC1 promotes skeletal muscle hypertrophy, but also drives organismal aging. Here, we address the question of whether mTORC1 activation or suppression is beneficial for skeletal muscle aging. We demonstrate that chronic mTORC1 inhibition with rapamycin is overwhelmingly, but not entirely, positive for aging mouse skeletal muscle, while genetic, muscle fiber-specific activation of mTORC1 is sufficient to induce molecular signatures of sarcopenia. Through integration of comprehensive physiological and extensive gene expression profiling in young and old mice, and following genetic activation or pharmacological inhibition of mTORC1, we establish the phenotypically-backed, mTORC1-focused, multi-muscle gene expression atlas, SarcoAtlas (https://sarcoatlas.scicore.unibas.ch/), as a user-friendly gene discovery tool. We uncover inter-muscle divergence in the primary drivers of sarcopenia and identify the neuromuscular junction as a focal point of mTORC1-driven muscle aging.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32908143 · DOI · PMC7481251
Sensory innervation in porous endplates by Netrin-1 from osteoclasts mediates PGE2-induced spinal hypersensitivity in mice [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Spinal pain is a major clinical problem, however, its origins and underlying mechanisms remain unclear.
- Closing excerpt
- These findings suggest that osteoclast-initiated porosity of endplates and sensory innervation are potential therapeutic targets for spinal pain.
- 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 (152 words)
Spinal pain is a major clinical problem, however, its origins and underlying mechanisms remain unclear. Here we report that in mice, osteoclasts induce sensory innervation in the porous endplates which contributes to spinal hypersensitivity in mice. Sensory innervation of the porous areas of sclerotic endplates in mice was confirmed. Lumbar spine instability (LSI), or aging, induces spinal hypersensitivity in mice. In these conditions, we show that there are elevated levels of PGE2 which activate sensory nerves, leading to sodium influx through Nav 1.8 channels. We show that knockout of PGE2 receptor 4 in sensory nerves significantly reduces spinal hypersensitivity. Inhibition of osteoclast formation by knockout Rankl in the osteocytes significantly inhibits LSI-induced porosity of endplates, sensory innervation, and spinal hypersensitivity. Knockout of Netrin-1 in osteoclasts abrogates sensory innervation into porous endplates and spinal hypersensitivity. These findings suggest that osteoclast-initiated porosity of endplates and sensory innervation are potential therapeutic targets for spinal pain.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31822662 · DOI · PMC6904550
Axonal TDP-43 condensates drive neuromuscular junction disruption through inhibition of local synthesis of nuclear encoded mitochondrial proteins [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Mislocalization of the predominantly nuclear RNA/DNA binding protein, TDP-43, occurs in motor neurons of ~95% of amyotrophic lateral sclerosis (ALS) patients, but the contribution of axonal TDP-43 to this neurodegenerative disease is unclear.
- Closing excerpt
- These findings support an axonal gain of function of TDP-43 in ALS, which can be targeted for therapeutic development.
- 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 (145 words)
Mislocalization of the predominantly nuclear RNA/DNA binding protein, TDP-43, occurs in motor neurons of ~95% of amyotrophic lateral sclerosis (ALS) patients, but the contribution of axonal TDP-43 to this neurodegenerative disease is unclear. Here, we show TDP-43 accumulation in intra-muscular nerves from ALS patients and in axons of human iPSC-derived motor neurons of ALS patient, as well as in motor neurons and neuromuscular junctions (NMJs) of a TDP-43 mislocalization mouse model. In axons, TDP-43 is hyper-phosphorylated and promotes G3BP1-positive ribonucleoprotein (RNP) condensate assembly, consequently inhibiting local protein synthesis in distal axons and NMJs. Specifically, the axonal and synaptic levels of nuclear-encoded mitochondrial proteins are reduced. Clearance of axonal TDP-43 or dissociation of G3BP1 condensates restored local translation and resolved TDP-43-derived toxicity in both axons and NMJs. These findings support an axonal gain of function of TDP-43 in ALS, which can be targeted for therapeutic development.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34824257 · DOI · PMC8617040
Age-Associated Dysregulation of Postsynaptic Mitochondria Perturbs Reinnervation Kinetics [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Age-associated degeneration of neuromuscular junctions (NMJs) contributes to sarcopenia and motor function decline, yet the mechanisms that drive this dysfunction in aging remain poorly defined.
- Closing excerpt
- These findings establish a critical role for postsynaptic mitochondrial integrity in sustaining NMJ stability and regenerative capacity and identify CHCH domain-containing proteins as key regulators of postsynaptic mitochondrial function during aging and injury.
- 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 (213 words)
Age-associated degeneration of neuromuscular junctions (NMJs) contributes to sarcopenia and motor function decline, yet the mechanisms that drive this dysfunction in aging remain poorly defined. Here, we demonstrate that postsynaptic mitochondria are significantly diminished in quantity in old-aged skeletal muscle, correlating with increased denervation and delayed reinnervation following nerve injury. Single-nucleus RNA sequencing before and after sciatic nerve crush from young and old-aged muscles further revealed that sub-synaptic myonuclei in old-aged muscle exhibit attenuated expression of mitochondrial gene programs, including oxidative phosphorylation, biogenesis, and import. To test whether these deficits are causal, we developed a muscle-specific CRISPR genome editing approach and targeted CHCHD2 and CHCHD10-two nuclear-encoded mitochondrial proteins that localize to the intermembrane space and interact with the mitochondrial contact site and cristae organizing system. CRISPR knockout of CHCHD2 and CHCHD10 in young muscle recapitulated old-aged muscle phenotypes, including mitochondrial disorganization, reduced ATP production, NMJ fragmentation, and delayed reinnervation. Transcriptional profiling of sub-synaptic myonuclei using single-nuclei RNA sequencing from CHCHD2 and CHCHD10 knockout muscles revealed impairments in activation of mitochondrial remodeling programs and elevated stress signatures when compared with controls. These findings establish a critical role for postsynaptic mitochondrial integrity in sustaining NMJ stability and regenerative capacity and identify CHCH domain-containing proteins as key regulators of postsynaptic mitochondrial function during aging and injury.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41496579 · DOI · PMC12775679
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 Diagnosis and management of Duchenne muscular dystrophy, part 1: diagnosis, and neuromuscular, rehabilitation, endocrine, and gastrointestinal and nutritional management [5]
- Research article Physiological and methodological considerations for the use of neuromuscular electrical stimulation [6]
- Research article Mechanisms Regulating Neuromuscular Junction Development and Function and Causes of Muscle Wasting [7]
- Research article The Mechanisms and Functions of Synaptic Facilitation [8]
- Research article Congenital myasthenic syndromes: pathogenesis, diagnosis, and treatment [9]
- Research article Neuromuscular Junction Formation, Aging, and Disorders [10]
References
- Ham DJ, Börsch A, Lin S, Thürkauf M, Weihrauch M, Reinhard JR, et al.. The neuromuscular junction is a focal point of mTORC1 signaling in sarcopenia. . 2020. PMID 32908143 · DOI · PMC7481251
- Ni S, Ling Z, Wang X, Cao Y, Wu T, Deng R, et al.. Sensory innervation in porous endplates by Netrin-1 from osteoclasts mediates PGE2-induced spinal hypersensitivity in mice. . 2019. PMID 31822662 · DOI · PMC6904550
- Altman T, Ionescu A, Ibraheem A, Priesmann D, Gradus-Pery T, Farberov L, et al.. Axonal TDP-43 condensates drive neuromuscular junction disruption through inhibition of local synthesis of nuclear encoded mitochondrial proteins. . 2021. PMID 34824257 · DOI · PMC8617040
- Guzman SD, Fraczek PM, Itsani K, Furati EK, Juros D, Kenney G, et al.. Age-Associated Dysregulation of Postsynaptic Mitochondria Perturbs Reinnervation Kinetics. . 2026. PMID 41496579 · DOI · PMC12775679
- Birnkrant DJ, Bushby K, Bann CM, Apkon SD, Blackwell A, Brumbaugh D, et al.. Diagnosis and management of Duchenne muscular dystrophy, part 1: diagnosis, and neuromuscular, rehabilitation, endocrine, and gastrointestinal and nutritional management. Lancet Neurol. 2018. PMID 29395989 · DOI · PMC5869704
- Maffiuletti NA. Physiological and methodological considerations for the use of neuromuscular electrical stimulation. Eur J Appl Physiol. 2010. PMID 20473619 · DOI
- Tintignac LA, Brenner HR, Rüegg MA. Mechanisms Regulating Neuromuscular Junction Development and Function and Causes of Muscle Wasting. Physiol Rev. 2015. PMID 26109340 · DOI
- Jackman SL, Regehr WG. The Mechanisms and Functions of Synaptic Facilitation. Neuron. 2017. PMID 28472650 · DOI · PMC5865607
- Engel AG, Shen XM, Selcen D, Sine SM. Congenital myasthenic syndromes: pathogenesis, diagnosis, and treatment. Lancet Neurol. 2015. PMID 25792100 · DOI · PMC4520251
- Li L, Xiong WC, Mei L. Neuromuscular Junction Formation, Aging, and Disorders. Annu Rev Physiol. 2018. PMID 29195055 · DOI
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.