ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Nerve injury induces a rapid efflux of nitric oxide (NO) detected with a novel NO microsensor.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 50 citations in OpenAlex.
- Carbon Anode in Carbon History.Molecules (Basel, Switzerland) · 2020Review
- Manganese Oxide Nanozymes Ameliorate Mechanical Allodynia in a Rat Model of Partial Sciatic Nerve-Transection Induced Neuropathic Pain.International journal of nanomedicine · 2019Article
- Metabolic oxygen consumption measurement with a single-cell biosensor after particle microbeam irradiation.Radiation and environmental biophysics · 2015Article
- 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
- 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
- Release and elementary mechanisms of nitric oxide in hair cells.Journal of neurophysiology · 2010Article
- Expanding the question-answering potential of single-cell microbeams at RARAF, USA.Journal of radiation research · 2009Review
- 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
- Three-dimensional culture of leech and snail ganglia for studies of neural repair.Invertebrate neuroscience : IN · 2005Article
- Repair and regeneration of functional synaptic connections: cellular and molecular interactions in the leech.Cellular and molecular neurobiology · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
An early step in repair of the leech CNS is the appearance of endothelial nitric oxide synthase (eNOS) immunoreactivity and NOS activity, but coincident generation of NO at the lesion after injury has not been shown. This is important because NO can regulate microglial cell motility and axon growth. Indirect measurement of NO with the standard citrulline assay demonstrated that NO was generated within 30 min after nerve cord injury. A polarographic NO-selective self-referencing microelectrode that measures NO flux noninvasively was developed to obtain higher spatial and temporal resolution. With this probe, it was possible to demonstrate that immediately after the leech CNS was injured, NO left the lesion with a mean peak efflux of 803 +/- 99 fmol NO cm(-2) sec(-1). NO efflux exponentially declined to a constant value, as described through the equation f(t) = y(o) + ae(-t/tau), with tau = 117 +/- 30 sec. The constant y(o) = 15.8 +/- 4.5 fmol cm(-2) represents a sustained efflux of NO. Approximately 200 pmol NO cm(-2) is produced at the lesion (n = 8). Thus, injury activates eNOS already present in the CNS and precedes the accumulation of microglia at the lesion, consistent with the hypothesis that NO acts to stop the migrating microglia at the lesion site.
Indexed as
Identifiers
11150338PMC6762443W1919995930What 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.