ArticleProceedings. Biological sciences1998
Injury-induced expression of endothelial nitric oxide synthase by glial and microglial cells in the leech central nervous system within minutes after injury.
Article in Proceedings. Biological sciences, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 41 citations in OpenAlex.
- Loss of cholinergic innervation differentially affects eNOS-mediated blood flow, drainage of Aβ and cerebral amyloid angiopathy in the cortex and hippocampus of adult mice.Acta neuropathologica communications · 2021Article
- A Comparative Biology of Microglia Across Species.Frontiers in cell and developmental biology · 2021Review
- 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
- Neuroglial ATP release through innexin channels controls microglial cell movement to a nerve injury.The Journal of general physiology · 2010Article
- Release and elementary mechanisms of nitric oxide in hair cells.Journal of neurophysiology · 2010Article
- ATP and NO dually control migration of microglia to nerve lesions.Developmental neurobiology · 2009Article
- Effects of nerve injury and segmental regeneration on the cellular correlates of neural morphallaxis.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2008Article
- Repair and regeneration of functional synaptic connections: cellular and molecular interactions in the leech.Cellular and molecular neurobiology · 2005Review
- Lymnaea epidermal growth factor promotes axonal regeneration in CNS organ culture.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- 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
- Nitric oxide influences injury-induced microglial migration and accumulation in the leech CNS.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
It is known that nitric oxide (NO) is produced by injured tissues of the mammalian central nervous system (CNS) within days of injury. The aim of the present experiments was to determine the cellular synthesis of NO in the CNS immediately after injury, using the CNS of the leech which is capable of synapse regeneration, as a step towards understanding the role of NO in nerve repair. We report that within minutes after crushing the nerve cord of the leech, the region of damage stained histochemically for NADPH diaphorase, which is indicative of nitric oxide synthase (NOS) activity, and was immunoreactive for endothelial NOS (eNOS). On immunoblots of leech CNS extract, the same antibody detected a band with a relative molecular mass of 140,000, which is approximately the size of vertebrate eNOS. Cells expressing eNOS immunoreactivity as a result of injury were identified after freezing nerve cords, a procedure that produced less tissue distortion than mechanical crushing. Immunoreactive cells included connective glia and some microglia. Calmodulin was necessary for the eNOS immunoreactivity: it was blocked by calmodulin antagonist W7 (25 microM), but not by similar concentrations of the less potent calmodulin antagonist W12. Thus in the leech CNS, in which axon and synapse regeneration is successful, an increase in NOS activity at lesions appears to be among the earliest responses to injury and may be important for repair of axons.
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Registered trials
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