Membrane-potential changes caused by 2,4-DNP and related phenols in resting crayfish axons are not due to uncoupling of mitochondria

Abstract

1. 1. The effects of 2,4-dinitrophenol (DNP) and six other phenols on the resting membrane potential and resistance of the crayfish medial giant axon were studied. 2. 2. DNP (5 × 10 −5−10 −3 M) caused a concentration-dependent depolarization up to 6 mV which at higher concentrations (1−5 × 10 −2 M) turned into a weak hyperpolarization. 3. 3. Taking into account the changes in membrane potential, the depolarization was accompanied by only slight changes in membrane resistance. The hyperpolarization occured together with a marked decrease in resistance suggesting an increase in resting potassium permeability. 4. 4. Phenol and most of the other derivatives (4-Cl; penta-Cl and 4-Cl-3, 5-di-CH 3) had qualitatively similar effects except for 2,4,6-trinitrophenol (TNP) which showed no depolarizing action. 5. 5. Neither of the membrane-potential effects is likely to be due to uncoupling of oxidative phosphorylation in mitochondria, since (a) the depolarizing action o DNP had a similar latency (about 5 sec) to that brought about by increasing the extracellular potassium concentration; and (b) TNP, which is known not to act as an uncoupler in intact mitochondria produced a prompt increase in the potassium permeability at a concentration in agreement with the relation between the potency and the octanol-water partition coefficient of the derivatives tested.