| pubmed-article:2554221 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2554221 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:2554221 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:2554221 | lifeskim:mentions | umls-concept:C0206441 | lld:lifeskim |
| pubmed-article:2554221 | lifeskim:mentions | umls-concept:C0019564 | lld:lifeskim |
| pubmed-article:2554221 | lifeskim:mentions | umls-concept:C1413038 | lld:lifeskim |
| pubmed-article:2554221 | pubmed:issue | 1-2 | lld:pubmed |
| pubmed-article:2554221 | pubmed:dateCreated | 1989-12-20 | lld:pubmed |
| pubmed-article:2554221 | pubmed:abstractText | In isolated rat hippocampal neurons, we observed 4 voltage- and extracellular Ca2+-dependent conductances; i.e. the T-, N- and L-type Ca2+ currents and tetrodotoxin-sensitive transient Ca2+ current. Intracellular perfusion with F- suppressed irreversibly the L-type Ca2+ current and partially the N-type one. omega-Conotoxin inhibited selectively the L-type Ca2+ current. Amiloride reduced strongly the T-type Ca2+ current without affecting the L-type one. Gd3+, nicardipine, phenytoin and octanol had no specific inhibition on the T-, N- and L-type Ca2+ currents. Thereby, the pharmacological property of mammalian CNS neurons for Ca2+ channel blockers considerably differs from that in the peripheral and cultured cells. | lld:pubmed |
| pubmed-article:2554221 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2554221 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2554221 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2554221 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2554221 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:2554221 | pubmed:issn | 0304-3940 | lld:pubmed |
| pubmed-article:2554221 | pubmed:author | pubmed-author:TakahashiKK | lld:pubmed |
| pubmed-article:2554221 | pubmed:author | pubmed-author:AkaikeNN | lld:pubmed |
| pubmed-article:2554221 | pubmed:author | pubmed-author:WakamoriMM | lld:pubmed |
| pubmed-article:2554221 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2554221 | pubmed:day | 25 | lld:pubmed |
| pubmed-article:2554221 | pubmed:volume | 104 | lld:pubmed |
| pubmed-article:2554221 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2554221 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2554221 | pubmed:pagination | 229-34 | lld:pubmed |
| pubmed-article:2554221 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:2554221 | pubmed:meshHeading | pubmed-meshheading:2554221-... | lld:pubmed |
| pubmed-article:2554221 | pubmed:year | 1989 | lld:pubmed |
| pubmed-article:2554221 | pubmed:articleTitle | Hippocampal CA1 pyramidal cells of rats have four voltage-dependent calcium conductances. | lld:pubmed |
| pubmed-article:2554221 | pubmed:affiliation | Department of Neurophysiology, Tohoku University School of Medicine, Sendai, Japan. | lld:pubmed |
| pubmed-article:2554221 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2554221 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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