| pubmed-article:17287339 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17287339 | lifeskim:mentions | umls-concept:C0000098 | lld:lifeskim |
| pubmed-article:17287339 | lifeskim:mentions | umls-concept:C0010656 | lld:lifeskim |
| pubmed-article:17287339 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
| pubmed-article:17287339 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:17287339 | lifeskim:mentions | umls-concept:C2261577 | lld:lifeskim |
| pubmed-article:17287339 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:17287339 | lifeskim:mentions | umls-concept:C2267219 | lld:lifeskim |
| pubmed-article:17287339 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:17287339 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:17287339 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:17287339 | pubmed:dateCreated | 2007-2-14 | lld:pubmed |
| pubmed-article:17287339 | pubmed:abstractText | 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine administration has been used, in various mammalian species, as an experimental model of Parkinson's disease. The pathogenesis for such pharmacologically induced Parkinson's disease involves 1-methyl-4-phenylpyridinium (MPP+), the active metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. This metabolite produces rapid degeneration of nigrostriatal dopaminergic neurons, which causes the parkinsonian syndrome. In this work, we show that injection of MPP+ into the presynaptic terminal of the squid giant synapse blocks synaptic transmission without affecting the presynaptic action potential or the presynaptic calcium currents. These effects of MPP+ were mimicked by the injection of an active form of caspase-3 and prevented by inhibitors of caspase-3 and protein kinase C delta. Ultrastructurally, MPP+-injected synapses showed a dramatic reduction in the number of neurotransmitter vesicles at the presynaptic active zone, as compared with control synapses. Otherwise, normal docking and clathrin-coated vesicles were observed, albeit at much reduced numbers. These results indicate that MPP+ acutely reduces presynaptic vesicular availability, not release, and that MPP+-induced pathogenesis results from presynaptic dysfunction that leads, secondarily, to dying-back neuropathy in affected neurons. | lld:pubmed |
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| pubmed-article:17287339 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17287339 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17287339 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17287339 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17287339 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:17287339 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:17287339 | pubmed:author | pubmed-author:MorfiniGerard... | lld:pubmed |
| pubmed-article:17287339 | pubmed:author | pubmed-author:BradyScott... | lld:pubmed |
| pubmed-article:17287339 | pubmed:author | pubmed-author:PiginoGustavo... | lld:pubmed |
| pubmed-article:17287339 | pubmed:author | pubmed-author:LlinásRodolfo... | lld:pubmed |
| pubmed-article:17287339 | pubmed:author | pubmed-author:MoreiraJorge... | lld:pubmed |
| pubmed-article:17287339 | pubmed:author | pubmed-author:SugimoriMutsu... | lld:pubmed |
| pubmed-article:17287339 | pubmed:author | pubmed-author:SerulleYafell... | lld:pubmed |
| pubmed-article:17287339 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17287339 | pubmed:day | 13 | lld:pubmed |
| pubmed-article:17287339 | pubmed:volume | 104 | lld:pubmed |
| pubmed-article:17287339 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17287339 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17287339 | pubmed:pagination | 2437-41 | lld:pubmed |
| pubmed-article:17287339 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:17287339 | pubmed:meshHeading | pubmed-meshheading:17287339... | lld:pubmed |
| pubmed-article:17287339 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17287339 | pubmed:articleTitle | 1-Methyl-4-phenylpyridinium induces synaptic dysfunction through a pathway involving caspase and PKCdelta enzymatic activities. | lld:pubmed |
| pubmed-article:17287339 | pubmed:affiliation | Program in Neuroscience and Physiology, New York University School of Medicine, New York, NY 10016, USA. | lld:pubmed |
| pubmed-article:17287339 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17287339 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17287339 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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