Effect of mitochondrial protein synthesis inhibitors on the trophic action of nerve stump in mice

Abstract

We studied the effect of mitochondrial protein synthesis inhibitors on the neurotrophic action of the nerve stump in mice. The sciatic nerve was cut as close to, or as far from the extensor digitorum longus muscles as possible. At 2 and 3 days after denervation, depolarization in the resting membrane potential of muscles with long nerve stumps (14–16 mm) was significantly smaller than in muscles with very short (<2 mm) nerve stumps. Chloramphenicol (100 mg/kg, p.o.), erythromycin (4 μg/kg, i.p.), ethidium bromide, (10 μg/kg, i.p.) or acridine (10 μg/kg, i.p.), administered for 2 or 3 days after denervation, increased depolarization in the resting membrane potential of muscles with long nerve stumps; muscles with very short nerve stumps were not affected by these drugs. The administration of chloramphenicol and erythromycin resulted in an earlier increase in the depolarization than ethidium bromide and acridine. Activities of cathepsin B and L of lysosomal proteases in the nerve stumps were enhanced by nerve degeneration; they were not affected by the administration of chloramphenicol or ethidium bromide. We suggest that proteins synthesized in mitochondria of the nerve may participate in trophic actions.