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Blocking Nitric Oxide Toxicity

  • Chapter
CNS Neuroprotection

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 155))

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Abstract

Nitric oxide (NO) is a novel neuronal messenger molecule which can mediate rapid signaling, diffusing freely in three dimensions to act throughout local regions of neural tissue (Garthwaite and Boulton 1995; Yun et al. 1996). NO and other nitrogen oxides are derived from chemical reactions following NOS activation. NO production can regulate ion channel activity, neurotransmitter release, cerebral blood flow, synaptic plasticity, growth cone structure, and gene expression in the nervous system. NO can elicit such diverse cellular signaling due to a wide variety of molecular targets including soluble guanylate cyclase, other heme-containing enzymes including cyclooxygenase, thiol moieties and tyrosine residues on proteins, iron sulfur-containing proteins, and superoxide anion. Thus, NO is important in normal neuronal signaling; however, when NO production is unregulated or excessive, NO can mediate neuronal degeneration. NO has been implicated in the neuropathology of stroke, trauma, AIDS dementia, Alzheimer’s disease, multiple sclerosis, as well as bacterial and viral encephalitis (Dawson and Snyder 1994; Meldrum 1996). Limiting NO production under pathologic conditions has become a potentially important therapeutic target for the treatment of various neurologic diseases and disorders.

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Sasaki, M., Dawson, T.M., Dawson, V.L. (2002). Blocking Nitric Oxide Toxicity. In: Marcoux, F.W., Choi, D.W. (eds) CNS Neuroprotection. Handbook of Experimental Pharmacology, vol 155. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-06274-6_6

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