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The NO Signaling Pathway in the Brain

Neural Injury, Neurological Disorders, and Aggression

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Book cover Cerebral Signal Transduction

Part of the book series: Contemporary Neuroscience ((CNEURO))

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Abstract

Nitric oxide (NO) is a widespread and multifunctional biological messenger molecule. It mediates vasodilation of blood vessels, host defense against infectious agents and tumors, and neurotransmission of the central and peripheral nervous systems (1–3). The discovery of NO as a messenger molecule in the nervous system also revised conventional concepts of neurotransmitters. Compared with the traditional neuronal messenger molecules, NO has a variety of distinguished features. NO is probably the smallest and most versatile bioactive molecule identified, it diffuses freely across membranes, it is not stored in synaptic vesicles, and it is not released by exocytosis upon membrane depolarization. NO seems to be terminated primarily by reactions with its targets. In the nervous system, NO may play a role not only in physiologic neuronal functions, such as neurotransmitter release, neural development, regeneration, synaptic plasticity, and regulation of gene expression, but also in pathological conditions in which deregulated excessive production of NO leads to neural injury. Furthermore, rapid progress is now being made in understanding the regulation of NOS activity and the cellular and molecular targets of NO under physiologic and pathologic conditions. Some of the newly revealed roles for NO in the nervous system include regulation or control of neuronal morphogenesis, short-term or long-term synaptic plasticity, regulation of gene expression, and modification of sexual and aggressive behavior. Excess formation of NO plays a role in neural injury in several kinds of neurologic insults, which has promoted the development of selective NOS inhibitors for the treatment of neurologic disorders.

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Sasaki, M., Dawson, V.L., Dawson, T.M. (2000). The NO Signaling Pathway in the Brain. In: Reith, M.E.A. (eds) Cerebral Signal Transduction. Contemporary Neuroscience. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-019-3_6

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