Source:http://linkedlifedata.com/resource/pubmed/id/10670441
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2000-3-1
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pubmed:abstractText |
It is demonstrated that not all voltage-gated calcium channel types expressed in neostriatal projection neurons (L, N, P, Q and R) contribute equally to the activation of calcium-dependent potassium currents. Previous work made clear that different calcium channel types contribute with a similar amount of current to whole-cell calcium current in neostriatal neurons. It has also been shown that spiny neurons possess both "big" and "small" types of calcium-dependent potassium currents and that activation of such currents relies on calcium entry through voltage-gated calcium channels. In the present work it was investigated whether all calcium channel types equally activate calcium-dependent potassium currents. Thus, the action of organic calcium channel antagonists was investigated on the calcium-activated outward current. Transient potassium currents were reduced by 4-aminopyridine and sodium currents were blocked by tetrodotoxin. It was found that neither 30 nM omega-Agatoxin-TK, a blocker of P-type channels, nor 200 nM calciseptine or 5 microM nitrendipine, blockers of L-type channels, were able to significantly reduce the outward current. In contrast, 400 nM omega-Agatoxin-TK, which at this concentration is able to block Q-type channels, and 1 microM omega-Conotoxin GVIA, a blocker of N-type channels, both reduced outward current by about 50%. These antagonists given together, or 500 nM omega-Conotoxin MVIIC, a blocker of N- and P/Q-type channels, reduced outward current by 70%. In addition, the N- and P/Q-type channel blockers preferentially reduce the afterhyperpolarization recorded intracellularly. The results show that calcium-dependent potassium channels in neostriatal neurons are preferentially activated by calcium entry through N- and Q-type channels in these conditions.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
0306-4522
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
95
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
745-52
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10670441-Animals,
pubmed-meshheading:10670441-Calcium,
pubmed-meshheading:10670441-Calcium Channel Blockers,
pubmed-meshheading:10670441-Calcium Channels,
pubmed-meshheading:10670441-Electric Conductivity,
pubmed-meshheading:10670441-Electrophysiology,
pubmed-meshheading:10670441-Neostriatum,
pubmed-meshheading:10670441-Neurons,
pubmed-meshheading:10670441-Potassium,
pubmed-meshheading:10670441-Rats,
pubmed-meshheading:10670441-Rats, Wistar
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pubmed:year |
2000
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pubmed:articleTitle |
Ca2+ channels that activate Ca2+-dependent K+ currents in neostriatal neurons.
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pubmed:affiliation |
Instituto de Fisiología Celular, UNAM, México City, DF, México.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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