Synaptosomal plasma and mitochondrial membrane potentials during anoxia.
The precise mechanism by which altered oxidative metabolism impairs neuronal function is unknown. Previous indirect studies suggest that anoxia's effects on the mitochondrial membrane potentials may underlie anoxia's actions. Twenty minutes of anoxia reduced the mitochondrial membrane potential of intact synaptosomes by 38-59 mV, but diminished the plasma membrane potential by only 4-10 mV. Anoxia did not alter the response of the plasma or mitochondrial membrane potentials to K+, nor did anoxia affect the reaction of the plasma membrane potential to valinomycin. However, anoxia diminished the response of the mitochondrial membrane potential to valinomycin by 50%. Thus, partial collapse of the mitochondrial membrane potential may be an important mediator of hypoxia-or anoxia-induced changes in neuronal function.
Gibson
G E
GE
Cornell University Medical College, Burke Medical Research Institute, White Plains, NY 10605.
Nielsen
P
P
Toral-Barza
L
L
D000693:Anaerobiosis; D000818:Animals; D001921:Brain / Q000502:physiology*; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology; D000860:Hypoxia; D007425:Intracellular Membranes / Q000187:drug effects / Q000502:physiology*; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D013574:Synaptosomes / Q000187:drug effects / Q000502:physiology*; D014634:Valinomycin / Q000494:pharmacology
D014634:Valinomycin; D011188:Potassium