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Nitric oxide signalling in the central nervous system Daisuke OKADA 1,2 1Laboratory for Cellular Information Processing, Brain Science Institute, RIKEN 2PRESTO, JST Keyword: 拡散 , NO合成酵素 , サイクリックGMP , ホスホジエステラーゼ pp.169-178
Published Date 1999/4/10
DOI https://doi.org/10.11477/mf.1431901036
  • Abstract
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The catalytic activity of neuronal nitric oxide synthase, which resembles the cytochrome P450-reductase complex, is regulated by calcium-calmodulin, tetrahydrobiopterin, and PDZ domain. Protein kinase C did not phosphorylate the stabilized dimer of neuronal nitric oxide synthase in vitro, suggesting that protein kinase C-dependent phosphorylation does not regulate neuronal nitric oxide synthase activity in neurons containing enough concentrations of tetrahydrobiopterin. Thus, nitric oxide synthase activation following neuronal excitation takes place through specific interactions in a spatiotemporally restricted manner. In contrast, due to ability to diffuse across cellular membranes and to react with multiple target molecules, nitric oxide has multiple functions indistributed area. Concentrations of nitric oxide that reach target molecules are regulated by rate and distribution of nitric oxide synthesis, target distribution, and potency of diffusion barriers. These characteristics enable nitric oxide to play unique roles as a signalling molecule in neuronal circuits. A novel technique monitoring intracellular phosphodiesterase activity suggested that nitric oxide triggered transient increases in cyclic GMP concentrations within neighboring cells. In cerebellar cortex, parallel fibers and basket cells are likely to release nitric oxide which triggers cyclic GMP production within Purkinje cells. These results suggest a role of cyclic GMP in the coincidence window of lone-term depression.


Copyright © 1999, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 1882-1243 印刷版ISSN 0001-8724 医学書院

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