ACTION OF METHYL FLUOROACETATE ON RESPIRATION AND POTENTIAL OF NERVE

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Abstract
Na fluoroacetate is almost inactive on frog sciatic nerve. Conduction is unaffected at 100 m[image] concn. and oxygen consumption is only 50% depressed. Lack of penetration does not adequately account for this feeble activity. Methyl fluoroacetate interferes with resting metabolism and leads to irreversible conduction block, large fibers before small ones, after a "latent" period during which threshold is rising. In summer frogs, more sensitive than winter ones, 5 m[image]. MFA blocks conduction in 3-4 hrs. by raising the threshold 2- to over 5-fold and slowing conduction 2-fold or more. Resting potential and spike height, for individual fibers, are not altered. Resting O2 consumption is cut to 70% normal by 1 m[image] MFA, to 20% by 5 m[image]; but the extra Qo2 of activity may remain intact when the resting value is severly cut. Fumarate and succinate can protect against MFA action; ethanol, acetate, pyruvate, alpha-ketoglutarate, and glucose are ineffective. These findings emphasize the safety factor in nerve metabolism and the metabolic difference between nerve and muscle, and support the existence and functional importance of a tricarboxylic cycle in nerve metabolism. The selective inhibition of resting rather than of active oxygen consumption, by MFA on nerve, is a unique reversal of the more usual selective inhibition of activity metabolism.

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