The peroxynitrite donor 3-morpholinosydnonimine induces reversible changes in electrophysiological properties of neurons of the guinea-pig spinal cord

Abstract Elevated concentrations of nitric oxide (NO) and peroxynitrite (ONOO− ) are present within the CNS following neurotrauma and are implicated in the pathogenesis of the accompanying neurologic deficits. We tested the hypothesis that elevated extracellular concentrations of ONOO− , introduced...

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Veröffentlicht in:	Neuroscience 2008-09, Vol.156 (1), p.107-117
Hauptverfasser:	Ashki, N, Hayes, K.C, Bao, F
Format:	Artikel
Sprache:	eng
Schlagworte:	Action Potentials - drug effects Action Potentials - physiology Animals axons Axons - drug effects Axons - metabolism Biological and medical sciences Cell Membrane - drug effects Cell Membrane - metabolism conduction Dose-Response Relationship, Drug Extracellular Fluid - drug effects Extracellular Fluid - metabolism Female Fundamental and applied biological sciences. Psychology Guinea Pigs immuno-fluorescence Molsidomine - analogs & derivatives Molsidomine - toxicity Nerve Degeneration - chemically induced Nerve Degeneration - metabolism Nerve Degeneration - physiopathology Neural Conduction - drug effects Neural Conduction - physiology Neurology Neurons - drug effects Neurons - metabolism Neurons - physiology neurotrauma nitric oxide Nitric Oxide - metabolism Nitric Oxide Donors - toxicity Nitro Compounds - metabolism Peroxynitrous Acid - agonists Peroxynitrous Acid - metabolism Peroxynitrous Acid - toxicity Sodium Channels - drug effects Sodium Channels - metabolism Spinal Cord - drug effects Spinal Cord - metabolism Spinal Cord - physiopathology Spinal Cord Injuries - drug therapy Spinal Cord Injuries - metabolism Spinal Cord Injuries - physiopathology spinal cord injury Tyrosine - analogs & derivatives Tyrosine - metabolism Vertebrates: nervous system and sense organs
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Zusammenfassung:	Abstract Elevated concentrations of nitric oxide (NO) and peroxynitrite (ONOO− ) are present within the CNS following neurotrauma and are implicated in the pathogenesis of the accompanying neurologic deficits. We tested the hypothesis that elevated extracellular concentrations of ONOO− , introduced by the donor 3-morpholinosydnonimine (SIN-1), induce reversible axonal conduction deficits in neurons of the guinea-pig spinal cord. The compound action potential (CAP) and compound membrane potential (CMP) of excised ventral cord white matter were recorded before, during, and after, bathing the tissue (30 min) in varying concentrations (0.125–2.0 mM) of SIN-1 ( 3.75–60 μM ONOO− ). The principal results were rapid onset, concentration-dependent, reductions in amplitude of the CAP ( P
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2008.06.050