Do K Q, Grima G, Benz B, Salt T E
Centre de Recherche en Neurosciences Psychiatriques, University of Lausanne, Prilly-Lausanne, Switzerland.
Ann N Y Acad Sci. 2002 May;962:81-92. doi: 10.1111/j.1749-6632.2002.tb04058.x.
The arginine-nitric oxide (Arg-NO) and the S-nitrosothiols systems, two less well-studied aspects of NO transmission in the central nervous system, are reviewed. A growing body of evidence suggested that they play a crucial role in NO synthesis and activity. l-Arginine, the NO precursor, is predominantly localized in glia. Together with in vitro and in vivo results of arginine release, this suggests a transfer of arginine from glia to neurons in order to supply NO synthase with its substrate. NO biosynthesis may thus involve the co-occurrence of the glial-neuronal transfer of arginine and of NOS activation. The arginine availability may shed light on the dual, beneficial and toxic effects of NO. At low arginine concentrations, neuronal NO synthase generates NO and superoxide, favouring the production of the toxin peroxynitrite. NMDA-induced excitotoxicity in neuronal cells is dependent on arginine availability and glia may play a neuroprotective role by supplying arginine. The reversible S-nitros(yl)ation of thiol containing molecules may represent an important cellular signal transduction mechanism, probably comparable to phosphorylation. S-nitrosothiols, in particular through the presence and release of S-nitroso-cysteinylglycine in sensory thalamus, may act as a local buffering system in NO transmission. This may represent a novel specific facilitating mechanism in order to enhance transmission of persistent stimuli.
