Neurobiology of Nitric Oxide

Yun, Hye Young; Dawson, Valina L.; Dawson, Ted M.

doi:10.1615/critrevneurobiol.v10.i3-4.20

Cited by 263 publications

(189 citation statements)

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“…In this study, we observed Ca 2+ ionophoreinduced generation of H 2 O 2 and caspase-3 activation, which were abolished by pretreatment with antioxidant. Cytoplasmic Ca 2+ overload can result in increased production of ROIs mediated by several mechanisms: activation of nitric oxide synthase (Yun et al, 1996), conversion of xanthine dehydrogenase to xanthine oxidase (Atlante et al, 1997), activation of phospholipase A 2 (Chan and Fishman, 1980), and increase of mitochondrial production of superoxide (Castilho et al, 1995). The ROIs-evoked membrane damage may induce further Ca 2+ influx and resultant accentuated Ca 2+ influx in turn will induce the generation of further ROIs.…”

Section: Discussionmentioning

confidence: 99%

Role of Ca(2+) in diallyl disulfide-induced apoptotic cell death of HCT-15 cells

Park

Kwon²,

Park³

et al. 2002

Exp Mol Med

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Section: Discussionmentioning

confidence: 99%

Role of Ca(2+) in diallyl disulfide-induced apoptotic cell death of HCT-15 cells

Park

Kwon²,

Park³

et al. 2002

Exp Mol Med

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“…bral ischaemia [43]. Importantly, the underlying pathology of ischaemia also favours uncoupled NOS-I catalysis and ROS formation owing to a variety of prevailing intracellular conditions, including decreased substrate availability [6] and lowered pH [44].…”

Section: Scheme 2 Autoinhibition Of Nos During Phase IImentioning

confidence: 99%

Autoinhibition of neuronal nitric oxide synthase: distinct effects of reactive nitrogen and oxygen species on enzyme activity

Kotsonis

Frey

Fröhlich

et al. 1999

Biochemical Journal

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Nitric oxide (NO) synthases (NOSs), which catalyse the oxidation of -arginine to -citrulline and an oxide of nitrogen, possibly NO or nitroxyl (NO − ), are subject to autoinhibition by a mechanism that has yet to be fully elucidated. In the present study we investigated the actions of NO and other NOS-derived products as possible autoregulators of enzyme activity. With the use of purified NOS-I, -arginine turnover was found to operate initially at V max (0-15 min, phase I) although, despite the presence of excess substrate and cofactors, prolonged catalysis (15-90 min, phase II) was associated with a rapid decline in -arginine turnover. Taken together, these observations suggested that one or more NOS products inactivate NOS. Indeed, exogenously applied reactive nitrogen oxide species (RNSs) decreased V max during phase I, although with different potencies (NO − NO ONOO − ) and efficacies (NO NO − l ONOO − ). The NO scavengers oxyhaemoglobin (HbO # ; 100 µM) and 1H-imidazol-1-yloxy-2-(4-carboxyphenyl)-4,5-dihydro-4,4,5,5-tetramethyl-3-

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“…The bioactive free radical NO is an important messenger involved in the development and maintenance of inflammation and pain (Yun et al, 1996). NO is generated by the activity of NO synthases (NOS) during the enzymatic conversion of L-arginine to L-citruliline.…”

Section: Introductionmentioning

confidence: 99%

Calcitonin gene-related peptide stimulation of nitric oxide synthesis and release from trigeminal ganglion glial cells

2008

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Clinical and basic science data support an integral role of calcitonin gene-related peptide (CGRP) in migraine pathology. Following trigeminal nerve activation, afferent release of CGRP causes vasodilation while efferent release leads to pain. Although CGRP can also be secreted from cell bodies of trigeminal neurons located within the ganglion, the function of CGRP released in the ganglion is poorly understood. Initially, we showed that SNAP-25, a protein required for CGRP release, was localized in cell bodies of trigeminal ganglia neurons. We also found that satellite glial cells in the ganglia express the CGRP1 receptor protein RAMP1. To determine whether CGRP could directly activate glial cells, primary cultures of rat trigeminal ganglia were utilized to study the effects of CGRP on glial nitric oxide (NO) synthesis and release. Under our culture conditions, >95% of the cells expressed glial fibrillary acidic protein and RAMP1. While weak iNOS staining was observed in glia under basal conditions, CGRP treatment greatly increased glial iNOS expression and NO release. This stimulatory effect was blocked by the CGRP1 receptor antagonist, CGRP 8-37 peptide. Treatment of glial cultures with forskolin or cAMP also increased iNOS expression and stimulated NO release to levels similar to CGRP. To our knowledge, this is the first evidence that activation of CGRP1 receptors regulates glial iNOS and NO release. We propose that following trigeminal nerve activation, CGRP secretion from neuronal cell bodies activates satellite glial cells that release NO and initiate inflammatory events in the ganglia that contribute to peripheral sensitization in migraine.

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Neurobiology of Nitric Oxide

Cited by 263 publications

References 0 publications

Role of Ca(2+) in diallyl disulfide-induced apoptotic cell death of HCT-15 cells

Role of Ca(2+) in diallyl disulfide-induced apoptotic cell death of HCT-15 cells

Autoinhibition of neuronal nitric oxide synthase: distinct effects of reactive nitrogen and oxygen species on enzyme activity

Calcitonin gene-related peptide stimulation of nitric oxide synthesis and release from trigeminal ganglion glial cells

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