| pubmed-article:1376999 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1376999 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
| pubmed-article:1376999 | lifeskim:mentions | umls-concept:C0205145 | lld:lifeskim |
| pubmed-article:1376999 | lifeskim:mentions | umls-concept:C0079883 | lld:lifeskim |
| pubmed-article:1376999 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:1376999 | lifeskim:mentions | umls-concept:C0030012 | lld:lifeskim |
| pubmed-article:1376999 | lifeskim:mentions | umls-concept:C0439855 | lld:lifeskim |
| pubmed-article:1376999 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:1376999 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:1376999 | pubmed:dateCreated | 1992-7-27 | lld:pubmed |
| pubmed-article:1376999 | pubmed:abstractText | Nitric oxide (NO) is an important messenger both systemically and in the CNS. In digital Ca2+ imaging and patch-clamp experiments, clinically available nitroso compounds that generate NO are shown to inhibit responses mediated by the NMDA subtype of the glutamate receptor on rat cortical neurons in vitro. A mechanism of action for this effect was investigated by using the specific NO-generating agent S-nitrosocysteine. We propose that free sulfhydryl groups on the NMDA receptor-channel complex react to form one or more S-nitrosothiols in the presence of NO. If vicinal thiol groups react in this manner, they can form a disulfide bond(s), which is thought to constitute the redox modulatory site of the receptor, resulting in a relatively persistent blockade of NMDA responses. These reactions with NO can afford protection from NMDA receptor-mediated neurotoxicity. Our results demonstrate a new pathway for NO regulation of physiological function that is not via cGMP, but instead involves reactions with membrane-bound thiol groups on the NMDA receptor-channel complex. | lld:pubmed |
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| pubmed-article:1376999 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1376999 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1376999 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1376999 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1376999 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:1376999 | pubmed:issn | 0896-6273 | lld:pubmed |
| pubmed-article:1376999 | pubmed:author | pubmed-author:KayR LRL | lld:pubmed |
| pubmed-article:1376999 | pubmed:author | pubmed-author:AggarwalS KSK | lld:pubmed |
| pubmed-article:1376999 | pubmed:author | pubmed-author:ChenH SHS | lld:pubmed |
| pubmed-article:1376999 | pubmed:author | pubmed-author:LiptonS ASA | lld:pubmed |
| pubmed-article:1376999 | pubmed:author | pubmed-author:HartmanJJ | lld:pubmed |
| pubmed-article:1376999 | pubmed:author | pubmed-author:YanQ HQH | lld:pubmed |
| pubmed-article:1376999 | pubmed:author | pubmed-author:SucherN JNJ | lld:pubmed |
| pubmed-article:1376999 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1376999 | pubmed:volume | 8 | lld:pubmed |
| pubmed-article:1376999 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1376999 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1376999 | pubmed:pagination | 1087-99 | lld:pubmed |
| pubmed-article:1376999 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:1376999 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1376999 | pubmed:articleTitle | Effect of nitric oxide production on the redox modulatory site of the NMDA receptor-channel complex. | lld:pubmed |
| pubmed-article:1376999 | pubmed:affiliation | Department of Neurology, Children's Hospital, Boston, Massachusetts. | lld:pubmed |
| pubmed-article:1376999 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1376999 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1376999 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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