Magnesium transport by brain mitochondria: energy requirement and dependence on Ca2+ fluxes.
The association of Mg2+ ions with mitochondria isolated from guinea pig cerebral cortex is investigated and resolved into two components, that bound to the surface of both the outer and the inner membranes and that transported into the mitochondrial matrix. When rotenone-treated mitochondria are preincubated in a Mg2+-containing medium, Mg2+ binding can be measured and actual Mg2+ transport determined after the addition of succinate. Mg2+ uptake as well as retention within mitochondria is an energy-dependent process linked to substrate oxidation. EGTA completely prevents Mg2+ uptake, while the Ca2+ uniporter inhibitor Ruthenium Red, along with prevention of Mg2+ uptake, induces a slow efflux of accumulated Mg2+ ions. These findings suggest that both inward and outward Mg2+ movements follow Ca2+ fluxes across the mitochondrial membrane. Modulation of Mg2+ movements by mitochondria is therefore suggested to occur within nerve terminals.
D000818:Animals; D001693:Biological Transport, Active; D001921:Brain / Q000378:metabolism*; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D004492:Edetic Acid / Q000494:pharmacology; D004734:Energy Metabolism; D006168:Guinea Pigs; D008274:Magnesium / Q000378:metabolism*; D008928:Mitochondria / Q000378:metabolism*; D013386:Succinates / Q000494:pharmacology; D019802:Succinic Acid; D013997:Time Factors
D013386:Succinates; D000001:Calcimycin; D004492:Edetic Acid; D019802:Succinic Acid; D008274:Magnesium; D002118:Calcium