Abstract
We show that nitric oxide (NO) from applied NO-donating chemicals induces collapse of ganglion cell axonal growth cones extending from explants of tadpole retina in culture. Peroxynitrite, a neurotoxic product of NO and superoxide reaction, did not induce collapse, and oxyhemoglobin, which binds NO, blocked the highly effective collapsing activity of the NO donor S-nitrosocysteine. Membrane-permeable analogs of cyclic guanosine monophosphate had no collapsing activity. Inhibitors of NO synthase did not induce collapse. NO is a potential retrograde messenger through which postsynaptic neurons signal to their inputs to modify synaptic efficacy following NMDA receptor activation. Our results suggest a role for NO as such a messenger during development of the retinotectal projection.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Axons / drug effects
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Cells, Cultured / cytology
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Cells, Cultured / drug effects
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Cells, Cultured / ultrastructure
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Cysteine / pharmacology
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Free Radical Scavengers / pharmacology
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Mercaptoethanol*
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Molsidomine / analogs & derivatives
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Molsidomine / pharmacology
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Neurites / drug effects*
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Nitrates / pharmacology
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Nitric Oxide / pharmacology*
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Nitrites / pharmacology
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Nitroprusside / pharmacology
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Nitroso Compounds / pharmacology
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Penicillamine / analogs & derivatives
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Penicillamine / pharmacology
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Retinal Ganglion Cells / cytology
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Retinal Ganglion Cells / drug effects*
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Retinal Ganglion Cells / ultrastructure
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S-Nitroso-N-Acetylpenicillamine
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S-Nitrosothiols*
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Signal Transduction / physiology
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Sulfhydryl Reagents / pharmacology
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Time Factors
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Vasodilator Agents / pharmacology
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Xenopus laevis
Substances
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Free Radical Scavengers
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Nitrates
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Nitrites
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Nitroso Compounds
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S-Nitrosothiols
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Sulfhydryl Reagents
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Vasodilator Agents
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Nitroprusside
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peroxynitric acid
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Nitric Oxide
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linsidomine
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Mercaptoethanol
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S-nitrosomercaptoethanol
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S-Nitroso-N-Acetylpenicillamine
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Molsidomine
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Penicillamine
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Cysteine