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Nerve conduction block by nitric oxide that is mediated by the axonal environment
P Shrager1, A W Custer, K Kazarinova
1Department of Neurobiology and Anatomy, University of Rochester Medical Center, Rochester, New York 14642, USA.
Journal of Neurophysiology
|April 18, 1998
Summary
Nitric oxide (NO) blocks nerve conduction in rats, especially in inflamed conditions. This effect depends on the nerve
Area of Science:
- Neuroscience
- Physiology
- Biochemistry
Background:
- Nitric oxide (NO) is a signaling molecule implicated in various physiological processes.
- Understanding NO's role in nerve function is crucial for neurological research.
Purpose of the Study:
- To investigate the effects of nitric oxide on peripheral nerve conduction.
- To explore the mechanisms and environmental dependencies of NO-induced nerve block.
Main Methods:
- Stimulated release of nitric oxide (NO) from diethylamine-NONOate (DEA-NONOate) in rat sciatic and vagus nerves.
- Recording of compound action potentials externally.
- Manipulation of nerve connective tissue sheaths (epineurium, endoneurium).
- Testing the effects of S-nitrosocysteine.
Main Results:
- NO exposure at inflammatory levels caused a complete, reversible loss of compound action potential in rat sciatic nerve.
- Loss of excitability was dependent on the axonal environment; removing endoneurial components reduced susceptibility.
- NO blocked action potentials in both myelinated and unmyelinated fibers of the vagus nerve.
- Nitrosothiol formation is a proposed mechanism, supported by S-nitrosocysteine's efficacy.
Conclusions:
- Nitric oxide reversibly blocks peripheral nerve conduction, with susceptibility influenced by the nerve's connective tissue.
- The findings suggest a potential role for NO in clinical deficits observed in nervous system inflammatory diseases.