ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Neuronal nitric oxide synthase plays a key role in CNS demyelination.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 103 citations in OpenAlex.
- Radical Revelations: The Interplay of Nitrosative Stress, the Endocannabinoid System, and Treatment of Age-Related Disorders.International journal of molecular sciences · 2026Review
- Multiple sclerosis: molecular pathogenesis and therapeutic intervention.Signal transduction and targeted therapy · 2025Review
- In Vitro Antioxidant and Anti-Neuroinflammatory Effects ofLife (Basel, Switzerland) · 2025Article
- Remyelination as a therapeutic target in the treatment of multiple sclerosis.AIMS neuroscience · 2025Review
- Tissue Hypoxia and Associated Innate Immune Factors in Experimental Autoimmune Optic Neuritis.International journal of molecular sciences · 2024Article
- Intrinsic organization of the corpus callosum.Frontiers in physiology · 2024Review
- Polysialic acid promotes remyelination in cerebellar slice cultures by Siglec-E-dependent modulation of microglia polarization.Frontiers in cellular neuroscience · 2023Article
- Effects of Venlafaxine, Risperidone and Febuxostat on Cuprizone-Induced Demyelination, Behavioral Deficits and Oxidative Stress.International journal of molecular sciences · 2021Article
- Nitric Oxide/Cyclic GMP-Dependent Calcium Signalling Mediates IL-6- and TNF-α-Induced Expression of Glial Fibrillary Acid Protein.Journal of molecular neuroscience : MN · 2021Article
- Coenzyme Q10 enhances remyelination and regulate inflammation effects of cuprizone in corpus callosum of chronic model of multiple sclerosis.Journal of molecular histology · 2021Article
- Exome-Wide Search for Genes Associated With Central Nervous System Inflammatory Demyelinating Diseases Following CHIKV Infection: The Tip of the Iceberg.Frontiers in genetics · 2021Article
- Effect and Mechanism of Catalpol on Remyelination via Regulation of the NOTCH1 Signaling Pathway.Frontiers in pharmacology · 2021Article
- Treatment With Tetrahydrobiopterin Improves White Matter Maturation in a Mouse Model for Prenatal Hypoxia in Congenital Heart Disease.Journal of the American Heart Association · 2019Article
- Five Decades of Cuprizone, an Updated Model to Replicate Demyelinating Diseases.Current neuropharmacology · 2019Review
- Pharmacological manipulation of cGMP and NO/cGMP in CNS drug discovery.Nitric oxide : biology and chemistry · 2019Review
- Substance P NK1 receptor in the rat corpus callosum during postnatal development.Brain and behavior · 2017Article
- Therapeutic inhibition of soluble brain TNF promotes remyelination by increasing myelin phagocytosis by microglia.JCI insight · 2017Article
- Crosstalk with Inflammatory Macrophages Shapes the Regulatory Properties of Multipotent Adult Progenitor Cells.Stem cells international · 2017Article
- Article
- Nitric Oxide: Exploring the Contextual Link with Alzheimer's Disease.Oxidative medicine and cellular longevity · 2016Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) is a small, short-lived molecule released from a variety of cells that is implicated in a multitude of biological processes. In pathological conditions, overproduction of NO may lead to the generation of highly reactive species, such as peroxynitrite and stable nitrosothiols, that may cause irreversible cell damage. Accordingly, several studies have suggested that NO may be involved in the pathogenesis of various neuroinflammatory/degenerative diseases. Increased concentrations of NO in the CNS in such cases are usually attributed to an increase in the inducible isoform of NO synthase (iNOS) usually produced by inflammatory cells. However, recent reports have suggested that the constitutive isoforms of NOS, neuronal (nNOS) and endothelial (eNOS), can also play a role. Here we examined the role that the constitutive isoforms of NOS might play in the cuprizone-induced model of demyelination/remyelination. Our results demonstrate that demyelination was greatly prevented in mice lacking nNOS. Protection was associated with a dramatic increase in mature oligodendrocyte survival and a decrease in apoptosis. Moreover, nNOS-/- mice did not respond to cuprizone with the extensive recruitment of microglia/macrophages and astrocytes, which is a typical feature in wild-type mice. Although demyelinating less, nNOS-/- mice exhibited a delay in remyelination. In eNOS-/- mice, demyelination progressed to the same extent as in wild type, but they showed a slight delay in spontaneous remyelination. In conclusion, this study highlights the importance of considering the source of NO when assessing its role in neuroinflammation/degeneration and emphasizes the differing pathological effects driven by the different NOS isoforms.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.