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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
1980-9-23
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pubmed:abstractText |
Mitochondria from guinea-pig cerebral cortex incubated in the presence of Pi or acetate are unable to regulate the extramitochondrial free Ca2+ at a steady-state which is independent of the Ca2+ accumulated in the matrix. This is due to the superimposition on kinetically regulated Ca2+ cycling of a membrane-potential-dependent reversal of the Ca2+ uniporter. The latter efflux is a consequence of a low membrane potential, which correlates with a loss of adenine nucleotide loss from the matrix, enable the mitochondria to maintain a high membrane potential and allow the mitochondria to buffer the extramitochondrial free Ca2+ precisely when up to 200 nmol of Ca2+/mg of protein is accumulated in the matrix. The steady-state extramitochondrial free Ca2+ is maintained as low as 0.3 microM. The Na+-activated efflux pathway is functional in the presence of ATP and oligomycin and accounts precisely for the change in steady-state free Ca2+ induced by Na+ addition. The need to distinguish carefully between kinetic and membrane-potential-dependent efflux pathways is emphasized and the competence of brain mitochondria to regulate cytosolic free Ca2+ concentrations in vivo is discussed.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-1093479,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-1175588,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-1252077,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-13330820,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-14257633,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-14299656,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-149027,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-151632,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-204287,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-213057,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-23291,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-25436,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-26681,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-27255,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-30376,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-30403,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-32035,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-320937,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-33670,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-348200,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-36390,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-4257941,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-437125,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-4429666,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-4448179,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-4452361,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-454375,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-4718807,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-4823433,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-4881885,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-4968800,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-5160741,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-639797,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-700162,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-729802,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-747647,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-8094,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7396840-872936
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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 |
Mar
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pubmed:issn |
0264-6021
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
186
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
833-9
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:7396840-Adenosine Triphosphate,
pubmed-meshheading:7396840-Animals,
pubmed-meshheading:7396840-Atractyloside,
pubmed-meshheading:7396840-Biological Transport,
pubmed-meshheading:7396840-Calcium,
pubmed-meshheading:7396840-Cerebral Cortex,
pubmed-meshheading:7396840-Female,
pubmed-meshheading:7396840-Guinea Pigs,
pubmed-meshheading:7396840-Kinetics,
pubmed-meshheading:7396840-Male,
pubmed-meshheading:7396840-Membrane Potentials,
pubmed-meshheading:7396840-Mitochondria,
pubmed-meshheading:7396840-Oligomycins,
pubmed-meshheading:7396840-Sodium
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pubmed:year |
1980
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pubmed:articleTitle |
The regulation of brain mitochondrial calcium-ion transport. The role of ATP in the discrimination between kinetic and membrane-potential-dependent calcium-ion efflux mechanisms.
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pubmed:publicationType |
Journal Article,
In Vitro
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