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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
1988-5-12
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pubmed:abstractText |
1. Calcium currents in cultured dorsal root ganglion (d.r.g.) cells were studied with the whole-cell patch-clamp technique. Using experimental conditions that suppressed Na+ and K+ currents, and 3-10 mM-external Ca2+ or Ba2+, we distinguished three distinct types of calcium currents (L, T and N) on the basis of voltage-dependent kinetics and pharmacology. 2. Component L activates at relatively positive test potentials (t.p. greater than -10 mV) and shows little inactivation during a 200 ms depolarization. It is completely reprimed at a holding potential (h.p.) of -60 mV, and can be isolated by using a more depolarized h.p. (-40 mV) to inactivate the other two types of calcium currents. 3. Component T can be seen in isolation with weak test pulses. It begins activating at potentials more positive than -70 mV and inactivates quickly and completely during a maintained depolarization (time constant, tau approximately 20-50 ms). The current amplitude and the rate of decay increase with stronger depolarizations until both reach a maximum at approximately -40 mV. Inactivation is complete at h.p. greater than -60 mV and is progressively removed between -60 and -95 mV. 4. Component N activates at relatively strong depolarizations (t.p. greater than -20 mV) and decays with time constants ranging from 50 to 110 ms. Inactivation is removed over a very broad range of holding potentials (h.p. between -40 and -110 mV). 5. With 10 mM-EGTA in the pipette solution, substitution of Ba2+ for Ca2+ as the charge carrier does not alter the rates of activation or relaxation of any component. However, T-type channels are approximately equally permeable to Ca2+ and Ba2+, while L-type and N-type channels are both much more permeable to Ba2+. 6. Component N cannot be explained by current-dependent inactivation of L current resulting from recruitment of extra L-type channels at negative holding potentials: raising the external Ba2+ concentration to 110 mM greatly increases the amplitude of L current evoked from h.p. = -30 mV but produces little inactivation. 7. Cadmium ions (20-50 microM) virtually eliminate both N and L currents (greater than 90% block) but leave T relatively unaffected (less than 50% block). 200 microM-Cd2+ blocks all three components. 8. Nickel ions (100 microM) strongly reduce T current but leave N and L current little changed. 9. The dihydropyridine antagonist nifedipine (10 microM) inhibits L current (approximately 60% block) at a holding potential that inactivates half the L-type channels.(ABSTRACT TRUNCATED AT 400 WORDS)
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-240906,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2409515,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2410795,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2410796,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2410797,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2411846,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2411919,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2419479,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2423955,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2428039,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2431263,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2436945,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2438698,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2578071,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2580308,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-2582115,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-4071055,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-6088117,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-6092622,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-6487739,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-6608056,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2451016-7441552
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
394
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
149-72
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:2451016-Animals,
pubmed-meshheading:2451016-Calcium,
pubmed-meshheading:2451016-Calcium Channel Blockers,
pubmed-meshheading:2451016-Cells, Cultured,
pubmed-meshheading:2451016-Chick Embryo,
pubmed-meshheading:2451016-Electrophysiology,
pubmed-meshheading:2451016-Ganglia, Spinal,
pubmed-meshheading:2451016-Ion Channels,
pubmed-meshheading:2451016-Kinetics,
pubmed-meshheading:2451016-Neurons, Afferent
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pubmed:year |
1987
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pubmed:articleTitle |
Kinetic and pharmacological properties distinguishing three types of calcium currents in chick sensory neurones.
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pubmed:affiliation |
Department of Physiology, Yale University School of Medicine, New Haven, CT 06510.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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