ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Nitric oxide influences injury-induced microglial migration and accumulation in the leech CNS.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed, 71 citations in OpenAlex.
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- Multiple sclerosis: molecular mechanisms and therapeutic opportunities.Antioxidants & redox signaling · 2013Review
- Arachidonic acid closes innexin/pannexin channels and thereby inhibits microglia cell movement to a nerve injury.Developmental neurobiology · 2013Article
- The leech nervous system: a valuable model to study the microglia involvement in regenerative processes.Clinical & developmental immunology · 2013Review
- Long-term nitric oxide exposure enhances lung cancer cell migration.BioMed research international · 2013Article
- Interaction of HmC1q with leech microglial cells: involvement of C1qBP-related molecule in the induction of cell chemotaxis.Journal of neuroinflammation · 2012Article
- Neuroglial ATP release through innexin channels controls microglial cell movement to a nerve injury.The Journal of general physiology · 2010Article
- ATP and NO dually control migration of microglia to nerve lesions.Developmental neurobiology · 2009Article
- Three-dimensional culture of leech and snail ganglia for studies of neural repair.Invertebrate neuroscience : IN · 2005Article
- Human and mouse microglia express connexin36, and functional gap junctions are formed between rodent microglia and neurons.Journal of neuroscience research · 2005Article
- Repair and regeneration of functional synaptic connections: cellular and molecular interactions in the leech.Cellular and molecular neurobiology · 2005Review
- Microglia-Müller glia cell interactions control neurotrophic factor production during light-induced retinal degeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Nerve injury induces a rapid efflux of nitric oxide (NO) detected with a novel NO microsensor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Damage to the leech or mammalian CNS increases nitric oxide (NO) production and causes accumulation of phagocytic microglial cells at the injury site. The aim of this study was to determine whether NO plays a role in microglial migration and accumulation at lesions in which NO is generated by a rapidly appearing endothelial nitric oxide synthase (eNOS) in leeches. Immunohistochemistry and cytochemistry demonstrated active eNOS before and throughout the period of microglial accumulation at the lesion. Decreasing NO synthesis by application of the NOS inhibitor N(w)-nitro-L-arginine methyl ester (1 mM) significantly reduced microglial accumulation, whereas its inactive enantiomer N(w)-nitro-D-arginine methyl ester (1 mM) resulted in microglial accumulation similar to that in crushed controls. Increasing NO with the donor spermine NONOate (SPNO) (1 mM) also inhibited accumulation, but not in the presence of the NO scavenger 2-(4-carboxyphenyl)-4,4,5, 5-teramethylimidazoline-oxyl-3-oxide (50 microM). The effect of SPNO was reversed by washout. SPNO application reduced average microglial migratory speeds and even reversibly arrested cell movement, as measured in living nerve cords. These results suggest that NO produced at a lesion may be a stop signal for microglia to accumulate there and that it can act on microglia early in their migration. Thus, NO may assume a larger role in nerve repair and recovery from injury by modulating accumulation of microglia, which appear to be important for axonal regeneration.
Indexed as
Identifiers
10648709PMC6774175W1485101683What OpenQuestion holds
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.