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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
1967-1-9
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pubmed:abstractText |
1. Motor nerve terminals in magnesium-poisoned rat hemidiaphragm-phrenic nerve preparations in vitro were stimulated with short depolarizing pulses of approximately threshold strength and the evoked antidromic responses recorded from the phrenic nerve. The percentage of these 1/sec or 0.5/sec stimuli to which there was no antidromic response was used as a quantitative measure of the terminal excitability. After standard tetanic stimulation (1000 impulses at 100/sec) the excitability of the terminals was depressed for an average duration of 60-70 sec, during most of which time no antidromic responses to stimuli of pretetanic intensity were recorded. There was no significant interaction between stimuli to the terminals at rates of 1 or 0.5/sec.2. Potassium-free solutions at first increased, then decreased, the post-tetanic depression of excitability. Raising [K](o) threefold (15 mM) abolished the post-tetanic depression and often converted it to an exaltation of excitability.3. Polarizing currents were applied to the terminals with a second electrode. Depolarizing currents increased, while hyperpolarizing currents decreased, the post-tetanic depression of excitability.4. In solutions with 70% of the normal NaCl content replaced by sucrose, the post-tetanic depression of excitability was reversibly prolonged.5. In the presence of 7.7 x 10(-6)M digoxin or 0.42 mM ouabain there was a small reversible reduction of post-tetanic excitability.6. After exposure to solutions containing no glucose or to solutions containing 3-5 mM sodium azide the excitability of the terminals was not altered by the tetanus. After washing with the control solution, post-tetanic depression of excitability returned. Antimycin-A (1.8 x 10(-6)M) had little or no effect upon post-tetanic excitability.7. It was concluded that the post-tetanic depression of excitability reflected hyperpolarization of the terminals and that this hyperpolarization was caused by a shift of the membrane potential towards the potassium equilibrium potential because of an increase in potassium permeability.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13142506,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13143186,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13278904,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13309347,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13320357,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13332599,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13332600,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13372787,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13417134,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13417139,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13525458,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13525676,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13564417,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13605983,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13769944,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13806927,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13819183,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13901551,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13908523,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-13955375,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-14043000,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-14167795,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-14250989,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-14263755,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-14284781,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-14324987,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-14368574,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-14449605,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-14449608,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-14861788,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-14946715,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-15406744,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-16991506,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-16993472,
http://linkedlifedata.com/resource/pubmed/commentcorrection/5921834-17104938
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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 |
May
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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 |
184
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
335-52
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:5921834-Animals,
pubmed-meshheading:5921834-Antimycin A,
pubmed-meshheading:5921834-Azides,
pubmed-meshheading:5921834-Digoxin,
pubmed-meshheading:5921834-Electric Stimulation,
pubmed-meshheading:5921834-Glucose,
pubmed-meshheading:5921834-Magnesium,
pubmed-meshheading:5921834-Motor Neurons,
pubmed-meshheading:5921834-Neuromuscular Junction,
pubmed-meshheading:5921834-Ouabain,
pubmed-meshheading:5921834-Phrenic Nerve,
pubmed-meshheading:5921834-Potassium,
pubmed-meshheading:5921834-Rats,
pubmed-meshheading:5921834-Sodium,
pubmed-meshheading:5921834-Sodium Chloride,
pubmed-meshheading:5921834-Sucrose
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pubmed:year |
1966
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pubmed:articleTitle |
The origin of the post-tetanic hyperpolarization of mammalian motor nerve terminals.
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pubmed:publicationType |
Journal Article
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