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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1995-12-12
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pubmed:abstractText |
After blockade of the voltage-dependent potassium conductances by intracellular application of 4-aminopyridine and tetraethylammonium in frog myelinated axons, a set of brief (0.1 ms) intracellular depolarizing pulses or a long (200 ms) depolarizing pulse evoked a train of action potentials. Under both experimental conditions a hyperpolarizing afterpotential appeared (duration 367 ms +/- 34, mean +/- S.E., n = 15). The purpose of this study was to investigate the properties of this hyperpolarizing afterpotential. It was found that the hyperpolarizing afterpotential increases in amplitude with: (1) the number of sodium-dependent action potentials; (2) action potential broadening (following potassium channels blockade); and (3) the level of depolarization during a current step. Application of tetrodotoxin prevented the activation of the hyperpolarizing afterpotential by any of the above stimuli. The hyperpolarizing afterpotential was unaffected by: (1) 8-acetyl-strophanthidin, an agent that poisons the electrogenic pumping in the axon; (2) blocking calcium influx with extracellular 10 mM magnesium or 2 mM manganese; and (3) buffering of the intracellular calcium, using EGTA in the recording microelectrode. Extracellular application of tetraethylammonium, but not 4-aminopyridine, reduced the hyperpolarizing afterpotential. The hyperpolarizing afterpotential reversed at >> -92 mV. Increasing the external potassium concentration from 2 to 10 mM shifted the reversal potential +14.5 mV, indicating that the hyperpolarizing afterpotential is a potassium mediated conductance.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Lithium,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Strophanthidin,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrodotoxin,
http://linkedlifedata.com/resource/pubmed/chemical/acetylstrophanthidin
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0306-4522
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
68
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
487-95
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7477959-Action Potentials,
pubmed-meshheading:7477959-Animals,
pubmed-meshheading:7477959-Axons,
pubmed-meshheading:7477959-Electric Stimulation,
pubmed-meshheading:7477959-Ganglia, Spinal,
pubmed-meshheading:7477959-Lithium,
pubmed-meshheading:7477959-Membrane Potentials,
pubmed-meshheading:7477959-Microelectrodes,
pubmed-meshheading:7477959-Nerve Fibers, Myelinated,
pubmed-meshheading:7477959-Potassium Channels,
pubmed-meshheading:7477959-Rana pipiens,
pubmed-meshheading:7477959-Sodium,
pubmed-meshheading:7477959-Strophanthidin,
pubmed-meshheading:7477959-Tetrodotoxin
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pubmed:year |
1995
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pubmed:articleTitle |
Evidence for a sodium-dependent potassium conductance in frog myelinated axon.
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pubmed:affiliation |
Department of Pharmacology and Therapeutics, McGill University, Montréal, Québec, Canada.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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