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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1996-12-13
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pubmed:abstractText |
Nitrogen oxides (NO) such as nitric oxide have been suggested to potentiate neurotransmitter release in a variety of neuronal cells. In this study, we showed that NO donors stimulate the release of noradrenaline (NA) from rat hippocampus both in vivo and in vitro. Co-addition of NO donors (sodium nitroprusside [SNP] or S-nitroso-N-acetylpenicillamine [SNAP]) and thiol compounds (dithiothreitol [DTT] or L-cysteine) stimulated [3H]NA release from prelabeled hippocampal slices. Microdialysis in freely moving rats was used to ascertain the role of NO in control of NA release from the hippocampus in vivo. Co-addition of SNAP and L-cysteine stimulated endogenous NA release within 30 min. The concentration of NA peaked between 30-60 min to almost 3 times basal level. Another thiol compound, glutathione, had no effect on [3H]NA release in the presence of SNP or SNAP. In the presence of SNAP, the effect of L-cysteine was much higher than that of the D-isomer, although SNAP did not show stereospecificity. The effect of SNAP/L-cysteine was rapid and the maximal increase in [3H]NA release was attained 0-1 min after application, which was similar in time course to the effect of KCI. Unlike the release by KCI, SNAP/L-cysteine-stimulated NA release was independent of extracellular CaCl2. However, pretreatment with the calmodulin antagonists W-7 or trifluoperazine significantly reduced the SNAP/L-cysteine-stimulated [3H]NA release. Formation of nitric oxide and activation of guanylate cyclase by nitric oxide were not responsible for SNAP/L-cysteine-stimulated NA release. These findings suggest that NO donors stimulate NA release from the hippocampus in the presence of thiol compounds such as L-cysteine in vivo and in vitro in a calmodulin-dependent, Ca(2+)-and cyclic GMP-independent manner. The physiological roles of thiol compounds such as L-cysteine or glutathione as intermediates of NO are discussed.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calmodulin,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic GMP,
http://linkedlifedata.com/resource/pubmed/chemical/Cysteine,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Penicillamine,
http://linkedlifedata.com/resource/pubmed/chemical/S-Nitroso-N-Acetylpenicillamine,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfhydryl Compounds
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0021-9541
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
169
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
87-96
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8841425-Animals,
pubmed-meshheading:8841425-Calmodulin,
pubmed-meshheading:8841425-Cyclic GMP,
pubmed-meshheading:8841425-Cysteine,
pubmed-meshheading:8841425-Enzyme Inhibitors,
pubmed-meshheading:8841425-Glutathione,
pubmed-meshheading:8841425-Hippocampus,
pubmed-meshheading:8841425-Male,
pubmed-meshheading:8841425-Nitric Oxide,
pubmed-meshheading:8841425-Norepinephrine,
pubmed-meshheading:8841425-Penicillamine,
pubmed-meshheading:8841425-Rats,
pubmed-meshheading:8841425-Rats, Wistar,
pubmed-meshheading:8841425-S-Nitroso-N-Acetylpenicillamine,
pubmed-meshheading:8841425-Stereoisomerism,
pubmed-meshheading:8841425-Sulfhydryl Compounds
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pubmed:year |
1996
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pubmed:articleTitle |
NO donors stimulate noradrenaline release from rat hippocampus in a calmodulin-dependent manner in the presence of L-cysteine.
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pubmed:affiliation |
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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