Nitric Oxide Signaling in the Central Nervous System

Nitric Oxide Signaling in the Central Nervous System nervous system (eNS) in 1988 (52), when it was identified as the unstable Nitric oxide (NO) was first recognized as a messenger molecule in the central intercellular factor that had been hypothesized, a year earlier (53), to mediate the increased cyclic GMP (cGMP) levels that occur on activation of glutamate receptors, particularly those of the NMDA (N-methyl-D-aspartate) subtype. The presence of an NO-forming enzyme (NO synthase, or NOS) in the brain was later confirmed (74), and this enzyme was subsequently purified (14) and its cDNA cloned and sequenced (12). The discovery that NO functions as a signaling molecule in the brain opened a new dimension in our concept of neural communication, one overlaying the classical picture of chemical neurotransmission, where information is passed between neuronal elements at discrete loci (synapses), and in one direction, with a diffusive type of signal that disregards the spatial constraints on neu­ rotransmitter activity normally imposed by membranes, transporters, and in­ activating enzymes. In principle, NO could spread out from its site of produc­ tion to influence many different tissue elements (neuronal, glial, and vascular) that are not necessarily in close anatomical juxtaposition. During the past few years, much information on the enzymology http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Physiology Annual Reviews

Nitric Oxide Signaling in the Central Nervous System

Annual Review of Physiology, Volume 57 (1) – Mar 1, 1995

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Publisher
Annual Reviews
Copyright
Copyright 1995 Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0066-4278
eISSN
1545-1585
DOI
10.1146/annurev.ph.57.030195.003343
pmid
7539993
Publisher site
See Article on Publisher Site

Abstract

nervous system (eNS) in 1988 (52), when it was identified as the unstable Nitric oxide (NO) was first recognized as a messenger molecule in the central intercellular factor that had been hypothesized, a year earlier (53), to mediate the increased cyclic GMP (cGMP) levels that occur on activation of glutamate receptors, particularly those of the NMDA (N-methyl-D-aspartate) subtype. The presence of an NO-forming enzyme (NO synthase, or NOS) in the brain was later confirmed (74), and this enzyme was subsequently purified (14) and its cDNA cloned and sequenced (12). The discovery that NO functions as a signaling molecule in the brain opened a new dimension in our concept of neural communication, one overlaying the classical picture of chemical neurotransmission, where information is passed between neuronal elements at discrete loci (synapses), and in one direction, with a diffusive type of signal that disregards the spatial constraints on neu­ rotransmitter activity normally imposed by membranes, transporters, and in­ activating enzymes. In principle, NO could spread out from its site of produc­ tion to influence many different tissue elements (neuronal, glial, and vascular) that are not necessarily in close anatomical juxtaposition. During the past few years, much information on the enzymology

Journal

Annual Review of PhysiologyAnnual Reviews

Published: Mar 1, 1995

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