Inscrição na biblioteca: Guest
Portal Digital Begell Biblioteca digital da Begell eBooks Diários Referências e Anais Coleções de pesquisa
Critical Reviews™ in Neurobiology
SJR: 0.121

ISSN Imprimir: 0892-0915
ISSN On-line: 2375-0014

Archives: Volume 10, 1996 to Volume 20, 2008

Critical Reviews™ in Neurobiology

DOI: 10.1615/CritRevNeurobiol.v12.i3.40
pages 223-243

Nitric Oxide in Cerebral Ischemic Neurodegeneration and Excitotoxicity

Paul J. L. M. Strijbos
Department of Molecular Neurobiology Research, SmithKline Beecham Pharmaceuticals, New Frontiers Science Park - North, Coldharbour Road, Harlow, Essex CM19 5AD, United Kingdom

RESUMO

The observation that the free radical nitric oxide (NO) acts as a cell signaling molecule in key physiological processes such as regulation of blood pressure and immunological host-defense responses is probably one of the most important and exciting findings made in biology in the last decade. Likewise, in the brain NO has been implicated in a number of fundamental processes, including memory formation, sexual behavior and the control of cerebral blood flow. This has radically altered the accepted dogma of brain physiology and has placed NO at the center stage of neuroscience research. Evidence suggests that some of the actions of NO in the brain may be intimately linked to those of the classic excitatory neurotransmitter glutamate. The historical view that aberrations in glutamate signal transduction may underlie central neurodegeneration following, for example, cerebral ischemia, has implicated NO, by default, as a potential mediator of neuronal death. Indeed, with the advent of potent and specific compounds that interact with NO synthesizing (NOS) enzymes and with the NO signaling cascade, there is now ample evidence to suggest that NO can mediate neurodegeneration, although its involvement is paradoxical. Its cerebrovascular effects may act to limit ischemic damage by preserving tissue perfusion and preventing platelet aggregation, while NO produced in the parenchyma, either directly following the ischemic insult or at a later stage as part of a neuroinflammatory response, may be deleterious to the outcome of ischemia. Nonetheless, significant efforts are made into the potential therapeutic use of chemical NO donors and specific NOS inhibitors in the treatment of cerebral ischemia and other central neurodegenerative disorders. Here, the latest concepts and developments in our understanding of the role of NO in cerebral ischemic neurodegeneration are discussed.


Articles with similar content:

Mitochondrial Permeability Transition as a Target for Ischemic Preconditioning
International Journal of Physiology and Pathophysiology, Vol.3, 2012, issue 2
Yulia P. Korkach, Yulia V. Goshovska, Vadim F. Sagach, Tetyana V Shimanskaya, Olena M. Rudyk
Downregulation of Gap Junctions in Cancer Cells
Critical Reviews™ in Oncogenesis, Vol.12, 2006, issue 3-4
Yasufumi Omori, Edward Leithe, Edgar Rivedal, Solveig Sirnes
Autophagy-Induced Drug Resistance in Liver Cancer
Critical Reviews™ in Oncogenesis, Vol.25, 2020, issue 1
Rama Rao Malla, Rahul Kumar Vempati
Efficacy of Ghrelin in Cancer Cachexia: Clinical Trials and a Novel Treatment by Rikkunshito
Critical Reviews™ in Oncogenesis, Vol.17, 2012, issue 3
Haruka Amitani, Naoki Fujitsuka, Tomohisa Hattori, Akio Inui, Akihiro Asakawa
Aberrant B-Raf Signaling in Human Cancer − 10 Years from Bench to Bedside
Critical Reviews™ in Oncogenesis, Vol.17, 2012, issue 1
Michael Roring, Tilman Brummer