| pubmed-article:18822346 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18822346 | lifeskim:mentions | umls-concept:C0019564 | lld:lifeskim |
| pubmed-article:18822346 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:18822346 | lifeskim:mentions | umls-concept:C1421168 | lld:lifeskim |
| pubmed-article:18822346 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:18822346 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
| pubmed-article:18822346 | pubmed:issue | 2-3 | lld:pubmed |
| pubmed-article:18822346 | pubmed:dateCreated | 2009-1-28 | lld:pubmed |
| pubmed-article:18822346 | pubmed:abstractText | Massive neuronal activation by glutamate can result in an excessive rise in cytoplasmic calcium, a process ultimately leading to neuronal death. We have investigated the role of the transient receptor potential channel 1 (TRPC1) in mediating glutamate-induced neuron death. We show that 2-APB (a blocker of store-operated Ca2+ entry) dramatically reduces glutamate-induced cell death in hippocampal organotypic slice cultures and that glutamate-induced toxicity is accompanied by an increase in TRPC1 expression. RNAi mediated knock-down ofTRPC1 in slice cultures prevented glutamate-induced cell death, indicating that TRPC1 plays a prominent role in calcium entry following exposure to glutamate. Thus, TRPC1 may represent a promising target for pharmacological interventions to prevent or reduce glutamate-induced neuronal damage. | lld:pubmed |
| pubmed-article:18822346 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18822346 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18822346 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18822346 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18822346 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:18822346 | pubmed:issn | 0304-3940 | lld:pubmed |
| pubmed-article:18822346 | pubmed:author | pubmed-author:UnsickerKlaus... | lld:pubmed |
| pubmed-article:18822346 | pubmed:author | pubmed-author:von Bohlen... | lld:pubmed |
| pubmed-article:18822346 | pubmed:author | pubmed-author:SubramaniamSr... | lld:pubmed |
| pubmed-article:18822346 | pubmed:author | pubmed-author:NarayananK... | lld:pubmed |
| pubmed-article:18822346 | pubmed:author | pubmed-author:IrmadyKrithiK | lld:pubmed |
| pubmed-article:18822346 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18822346 | pubmed:day | 3 | lld:pubmed |
| pubmed-article:18822346 | pubmed:volume | 446 | lld:pubmed |
| pubmed-article:18822346 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18822346 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18822346 | pubmed:pagination | 117-22 | lld:pubmed |
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| pubmed-article:18822346 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18822346 | pubmed:articleTitle | Evidence that TRPC1 is involved in hippocampal glutamate-induced cell death. | lld:pubmed |
| pubmed-article:18822346 | pubmed:affiliation | Interdisciplinary Centerfor Neurosciences (IZN), Department of Neuroanatomy, University of Heidelberg, Im Neuenheimer Feld 307, D-69120 Heidelberg, Germany. | lld:pubmed |
| pubmed-article:18822346 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18822346 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:22063 | entrezgene:pubmed | pubmed-article:18822346 | lld:entrezgene |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:18822346 | lld:pubmed |
