REGULATION OF BRAIN MITOCHONDRIAL CALCIUM-ION TRANSPORT - ROLE OF ATP IN THE DISCRIMINATION BETWEEN KINETIC AND MEMBRANE-POTENTIAL-DEPENDENT CALCIUM-ION EFFLUX MECHANISMS
REGULATION OF BRAIN MITOCHONDRIAL CALCIUM-ION TRANSPORT - ROLE OF ATP IN THE DISCRIMINATION BETWEEN KINETIC AND MEMBRANE-POTENTIAL-DEPENDENT CALCIUM-ION EFFLUX MECHANISMS
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DOI:
10.1042/bj1860833
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发表时间:
1980-01-01
影响因子:
4.1
通讯作者:
SCOTT, ID
中科院分区:
文献类型:
--
作者:
NICHOLLS, DG;SCOTT, ID
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 nucleotides from the matrix. Low concentrations of ATP prevent 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 .mu.M. 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.