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 (628 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
Differentiated tissue of the central nervous system composed of nerve cells, fibers, dendrites, and specialized supporting cells.
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: Nerve Tissues; Tissue, Nerve; Tissues, Nerve; Nervous Tissue; Nervous Tissues; Tissue, Nervous; Tissues, Nervous.
Where it fits in the MeSH classification
- Broader topics
- Tissues
- Narrower topics
- Ependyma; Myelin Sheath
Related concepts
Research landscape
PubMed indexes 30,634 records tagged with the MeSH heading “Nerve Tissue” (counts retrieved 2026-10-31). 3,690 of them (12.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 16,844 records.
Reviews account for 3,184 records (10.4%) and meta-analyses for 17. Randomized controlled trials number 37 (0.1%) 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 | 16,844 |
| 2000-2009 | 4,411 |
| 2010-2019 | 5,689 |
| 2020 onward | 3,690 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 3,184 | 10.4% |
| Meta-analyses | 17 | 0.1% |
| Randomized controlled trials | 37 | 0.1% |
Method: PubMed query "Nerve Tissue"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
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 |
|---|---|---|---|---|
| Adipo-glial signaling mediates metabolic adaptation in peripheral nerve regeneration | 2023 | Research article Design not recorded in structured metadata | 84 | cc by PMID 37989315 · DOI · PMC10722468 |
| Oligodendrocytes and myelin limit neuronal plasticity in visual cortex | 2024 | Research article Design not recorded in structured metadata | 74 | cc by PMID 39169185 · DOI · PMC11424474 |
| Oligodendrocyte calcium signaling promotes actin-dependent myelin sheath extension | 2024 | Research article Design not recorded in structured metadata | 45 | cc by PMID 38177161 · DOI · PMC10767123 |
| Myelin sheaths in the central nervous system can withstand damage and dynamically remodel | 2026 | Research article Design not recorded in structured metadata | 9 | cc by PMID 41678629 · DOI · PMC7618902 |
Adipo-glial signaling mediates metabolic adaptation in peripheral nerve regeneration [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The peripheral nervous system harbors a remarkable potential to regenerate after acute nerve trauma.
- Closing excerpt
- Our findings propose a model according to which acute nerve injury triggers a therapeutically targetable intercellular crosstalk that modulates glial metabolism to provide sufficient energy for successful nerve repair.
- 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 (140 words)
The peripheral nervous system harbors a remarkable potential to regenerate after acute nerve trauma. Full functional recovery, however, is rare and critically depends on peripheral nerve Schwann cells that orchestrate breakdown and resynthesis of myelin and, at the same time, support axonal regrowth. How Schwann cells meet the high metabolic demand required for nerve repair remains poorly understood. We here report that nerve injury induces adipocyte to glial signaling and identify the adipokine leptin as an upstream regulator of glial metabolic adaptation in regeneration. Signal integration by leptin receptors in Schwann cells ensures efficient peripheral nerve repair by adjusting injury-specific catabolic processes in regenerating nerves, including myelin autophagy and mitochondrial respiration. Our findings propose a model according to which acute nerve injury triggers a therapeutically targetable intercellular crosstalk that modulates glial metabolism to provide sufficient energy for successful nerve repair.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37989315 · DOI · PMC10722468
Oligodendrocytes and myelin limit neuronal plasticity in visual cortex [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Developmental myelination is a protracted process in the mammalian brain1.
- Closing excerpt
- These results establish a critical role for oligodendrocytes in shaping the maturation and stabilization of cortical circuits and support the concept of developmental myelination acting as a functional brake on neuronal plasticity.
- 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 (189 words)
Developmental myelination is a protracted process in the mammalian brain1. One theory for why oligodendrocytes mature so slowly posits that myelination may stabilize neuronal circuits and temper neuronal plasticity as animals age2-4. We tested this theory in the visual cortex, which has a well-defined critical period for experience-dependent neuronal plasticity5. During adolescence, visual experience modulated the rate of oligodendrocyte maturation in visual cortex. To determine whether oligodendrocyte maturation in turn regulates neuronal plasticity, we genetically blocked oligodendrocyte differentiation and myelination in adolescent mice. In adult mice lacking adolescent oligodendrogenesis, a brief period of monocular deprivation led to a significant decrease in visual cortex responses to the deprived eye, reminiscent of the plasticity normally restricted to adolescence. This enhanced functional plasticity was accompanied by a greater turnover of dendritic spines and coordinated reductions in spine size following deprivation. Furthermore, inhibitory synaptic transmission, which gates experience-dependent plasticity at the circuit level, was diminished in the absence of adolescent oligodendrogenesis. These results establish a critical role for oligodendrocytes in shaping the maturation and stabilization of cortical circuits and support the concept of developmental myelination acting as a functional brake on neuronal plasticity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39169185 · DOI · PMC11424474
Oligodendrocyte calcium signaling promotes actin-dependent myelin sheath extension [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Myelin is essential for rapid nerve signaling and is increasingly found to play important roles in learning and in diverse diseases of the CNS.
- Closing excerpt
- Together, our work reveals a cellular mechanism required for accurate CNS myelin formation and may provide mechanistic insight into how oligodendrocytes respond to neuronal activity to sculpt and refine myelin sheaths.
- 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 (174 words)
Myelin is essential for rapid nerve signaling and is increasingly found to play important roles in learning and in diverse diseases of the CNS. Morphological parameters of myelin such as sheath length are thought to precisely tune conduction velocity, but the mechanisms controlling sheath morphology are poorly understood. Local calcium signaling has been observed in nascent myelin sheaths and can be modulated by neuronal activity. However, the role of calcium signaling in sheath formation remains incompletely understood. Here, we use genetic tools to attenuate oligodendrocyte calcium signaling during myelination in the developing mouse CNS. Surprisingly, genetic calcium attenuation does not grossly affect the number of myelinated axons or myelin thickness. Instead, calcium attenuation causes myelination defects resulting in shorter, dysmorphic sheaths. Mechanistically, calcium attenuation reduces actin filaments in oligodendrocytes, and an intact actin cytoskeleton is necessary and sufficient to achieve accurate myelin morphology. Together, our work reveals a cellular mechanism required for accurate CNS myelin formation and may provide mechanistic insight into how oligodendrocytes respond to neuronal activity to sculpt and refine myelin sheaths.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38177161 · DOI · PMC10767123
Myelin sheaths in the central nervous system can withstand damage and dynamically remodel [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Myelin damage is a hallmark of several neurological disorders, but how it occurs remains to be fully understood.
- Closing excerpt
- Our data indicate that myelin swelling is a conserved feature of demyelination and that damage to myelin sheaths can resolve, opening opportunities for targeting human disease.
- 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 (125 words)
Myelin damage is a hallmark of several neurological disorders, but how it occurs remains to be fully understood. In this study, we found that early damage in zebrafish and rodent demyelination models is characterized by myelin swelling. We show, through live imaging, that myelin swelling does not always lead to myelin loss and that swellings can sometimes resolve, allowing sheaths to remodel. Increased neuronal activity during early demyelination exacerbates myelin damage, whereas reducing neuronal activity mitigates myelin swelling in both zebrafish and mice. In human multiple sclerosis tissue, myelin swelling is also dynamic and is prominent around active lesions. Our data indicate that myelin swelling is a conserved feature of demyelination and that damage to myelin sheaths can resolve, opening opportunities for targeting human disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41678629 · DOI · PMC7618902
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 Myelination of the nervous system: mechanisms and functions [5]
- Research article Oligodendrocytes: Myelination and Axonal Support [6]
- Research article White matter changes in Alzheimer's disease: a focus on myelin and oligodendrocytes [7]
- Research article Myelin in the Central Nervous System: Structure, Function, and Pathology [8]
- Research article Regenerating CNS myelin - from mechanisms to experimental medicines [9]
- Research article Oligodendrocytes in Development, Myelin Generation and Beyond [10]
References
- Sundaram VK, Schütza V, Schröter NH, Backhaus A, Bilsing A, Joneck L, et al.. Adipo-glial signaling mediates metabolic adaptation in peripheral nerve regeneration. . 2023. PMID 37989315 · DOI · PMC10722468
- Xin W, Kaneko M, Roth RH, Zhang A, Nocera S, Ding JB, et al.. Oligodendrocytes and myelin limit neuronal plasticity in visual cortex. . 2024. PMID 39169185 · DOI · PMC11424474
- Iyer M, Kantarci H, Cooper MH, Ambiel N, Novak SW, Andrade LR, et al.. Oligodendrocyte calcium signaling promotes actin-dependent myelin sheath extension. . 2024. PMID 38177161 · DOI · PMC10767123
- Arafa D, van de Korput J, Braaker PN, Higgins KP, Meijns NRC, Marshall-Phelps KLH, et al.. Myelin sheaths in the central nervous system can withstand damage and dynamically remodel. . 2026. PMID 41678629 · DOI · PMC7618902
- Nave KA, Werner HB. Myelination of the nervous system: mechanisms and functions. Annu Rev Cell Dev Biol. 2014. PMID 25288117 · DOI
- Simons M, Nave KA. Oligodendrocytes: Myelination and Axonal Support. Cold Spring Harb Perspect Biol. 2015. PMID 26101081 · DOI · PMC4691794
- Nasrabady SE, Rizvi B, Goldman JE, Brickman AM. White matter changes in Alzheimer's disease: a focus on myelin and oligodendrocytes. Acta Neuropathol Commun. 2018. PMID 29499767 · DOI · PMC5834839
- Stadelmann C, Timmler S, Barrantes-Freer A, Simons M. Myelin in the Central Nervous System: Structure, Function, and Pathology. Physiol Rev. 2019. PMID 31066630 · DOI
- Franklin RJM, Ffrench-Constant C. Regenerating CNS myelin - from mechanisms to experimental medicines. Nat Rev Neurosci. 2017. PMID 29142295 · DOI
- Kuhn S, Gritti L, Crooks D, Dombrowski Y. Oligodendrocytes in Development, Myelin Generation and Beyond. Cells. 2019. PMID 31726662 · DOI · PMC6912544
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 2026-10-31.
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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.