pubmed-article:15256739 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15256739 | lifeskim:mentions | umls-concept:C0235032 | lld:lifeskim |
pubmed-article:15256739 | lifeskim:mentions | umls-concept:C0001128 | lld:lifeskim |
pubmed-article:15256739 | lifeskim:mentions | umls-concept:C1152715 | lld:lifeskim |
pubmed-article:15256739 | lifeskim:mentions | umls-concept:C0728938 | lld:lifeskim |
pubmed-article:15256739 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
pubmed-article:15256739 | lifeskim:mentions | umls-concept:C1721800 | lld:lifeskim |
pubmed-article:15256739 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:15256739 | pubmed:dateCreated | 2004-7-16 | lld:pubmed |
pubmed-article:15256739 | pubmed:abstractText | Neurolathyrism is a human motoneuron disease caused by the overconsumption of grass pea (Lathyrus sativus) that contains a toxic non-protein amino acid, 3-N-oxalyl-L-2,3-diaminopropanoic acid (L-beta-ODAP). The preventive activities of various glutamatergic agents from acute neuronal death caused by L-beta-ODAP were studied using rat primary cortical neuron/glia culture. Nearly 80% of the rat primary cortical neurons were killed by 300 microM L-beta-ODAP within 24 h. Though antagonists acting on the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor prevented most of the toxicity, antagonists acting on group I metabotropic glutamatergic receptors (mGluRs), including (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA), (S)-alpha-methyl-4-carboxyphenylglycine (MCPG), and 2-methyl-6-(2-phenylethenyl)pyridine (SIB1893) partially and significantly prevented neuronal death due to L-beta-ODAP. These antagonists, within limited concentrations, did not have any inhibitory effects on the currents through AMPA receptors expressed in Xenopus oocytes. L-beta-ODAP itself did not induce the currents through group I mGluRs expressed in Xenopus oocytes. These results suggest that the neurotoxicity induced by L-beta-ODAP is partially mediated by the activation of group I mGluRs by an indirect mechanisms. | lld:pubmed |
pubmed-article:15256739 | pubmed:language | eng | lld:pubmed |
pubmed-article:15256739 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15256739 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:15256739 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15256739 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15256739 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15256739 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15256739 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15256739 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15256739 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15256739 | pubmed:month | Jul | lld:pubmed |
pubmed-article:15256739 | pubmed:issn | 0918-6158 | lld:pubmed |
pubmed-article:15256739 | pubmed:author | pubmed-author:WatanabeKazuk... | lld:pubmed |
pubmed-article:15256739 | pubmed:author | pubmed-author:LambeinFernan... | lld:pubmed |
pubmed-article:15256739 | pubmed:author | pubmed-author:YamamotoMakot... | lld:pubmed |
pubmed-article:15256739 | pubmed:author | pubmed-author:IkegamiFumioF | lld:pubmed |
pubmed-article:15256739 | pubmed:author | pubmed-author:MasukoTakashi... | lld:pubmed |
pubmed-article:15256739 | pubmed:author | pubmed-author:IgarashiKazue... | lld:pubmed |
pubmed-article:15256739 | pubmed:author | pubmed-author:KusamaTadashi... | lld:pubmed |
pubmed-article:15256739 | pubmed:author | pubmed-author:Kusama-Eguchi... | lld:pubmed |
pubmed-article:15256739 | pubmed:author | pubmed-author:KuoYu-HaeyYH | lld:pubmed |
pubmed-article:15256739 | pubmed:author | pubmed-author:SudaAtsuhiroA | lld:pubmed |
pubmed-article:15256739 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15256739 | pubmed:volume | 27 | lld:pubmed |
pubmed-article:15256739 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15256739 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15256739 | pubmed:pagination | 1052-8 | lld:pubmed |
pubmed-article:15256739 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:15256739 | pubmed:year | 2004 | lld:pubmed |
pubmed-article:15256739 | pubmed:articleTitle | Partial involvement of group I metabotropic glutamate receptors in the neurotoxicity of 3-N-oxalyl-L-2,3-diaminopropanoic acid (L-beta-ODAP). | lld:pubmed |
pubmed-article:15256739 | pubmed:affiliation | Laboratory of Biology, College of Pharmacy, Nihon University, Japan. kusamak@pha.nihon-u.ac.jp | lld:pubmed |
pubmed-article:15256739 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15256739 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:15256739 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |