| pubmed-article:1321648 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1321648 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:1321648 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:1321648 | lifeskim:mentions | umls-concept:C0682700 | lld:lifeskim |
| pubmed-article:1321648 | lifeskim:mentions | umls-concept:C0752247 | lld:lifeskim |
| pubmed-article:1321648 | lifeskim:mentions | umls-concept:C0205099 | lld:lifeskim |
| pubmed-article:1321648 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:1321648 | pubmed:dateCreated | 1992-8-27 | lld:pubmed |
| pubmed-article:1321648 | pubmed:abstractText | The peptide toxin omega-Aga-IVA blocked P-type Ca2+ channel current in rat Purkinje neurons (KD approximately 2 nM) but had no effect on identified T-type, L-type, or N-type currents in a variety of central and peripheral neurons. omega-Aga-IVA blocked a substantial fraction of high threshold Ca2+ channel current in neurons from the hippocampal CA1 region (mean 26%), visual cortex (32%), spinal cord (45%), and dorsal root ganglia (23%), but less in hippocampal CA3 neurons (14%) and none in sympathetic neurons. In all cases, omega-Aga-IVA block could be reversed by a brief train of strong depolarizations. There was no overlap between current blocked by omega-Aga-IVA and the fractions blocked by dihydropyridines and omega-conotoxin GVIA, but not all current resistant to dihydropyridines and omega-conotoxin was blocked by omega-Aga-IVA. The results suggest that omega-Aga-IVA is highly selective for P-type channels and that many central neurons and some peripheral neurons possess substantial P-type current. | lld:pubmed |
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| pubmed-article:1321648 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:1321648 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1321648 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1321648 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:1321648 | pubmed:issn | 0896-6273 | lld:pubmed |
| pubmed-article:1321648 | pubmed:author | pubmed-author:AdamsM EME | lld:pubmed |
| pubmed-article:1321648 | pubmed:author | pubmed-author:BeanB PBP | lld:pubmed |
| pubmed-article:1321648 | pubmed:author | pubmed-author:MintzI MIM | lld:pubmed |
| pubmed-article:1321648 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1321648 | pubmed:volume | 9 | lld:pubmed |
| pubmed-article:1321648 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1321648 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1321648 | pubmed:pagination | 85-95 | lld:pubmed |
| pubmed-article:1321648 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:1321648 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1321648 | pubmed:articleTitle | P-type calcium channels in rat central and peripheral neurons. | lld:pubmed |
| pubmed-article:1321648 | pubmed:affiliation | Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115. | lld:pubmed |
| pubmed-article:1321648 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1321648 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1321648 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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