Free radical mechanism for phenylhydrazine action on the retractor unguis muscle of the grasshopper, Romalea microptera

Abstract

1. 1. When autoxidation was prevented by 10 −4 M ascorbate and EDTA, phenylhydrazine (10 −3 M) only slightly and reversibly diminished the neurally evoked contractions of the retractor unguis muscle of the grasshopper, Romalea microptera. 2. 2. When 10 −3 M phenylhydrazine solutions were in the course of oxidation, they completely and irreversibly abolished the contractile response, the excitatory postsynaptic potential, and the graded, electrically excited potential. The resting potential also was diminished. These effects were apparently induced by the free radical intermediates of oxidation. 3. 3. Once oxidation was completed, 10 −4 M phenylhydrazine potentiated the contractions. Benzene (5 × 10 −5 M), an oxidation product of phenylhydrazine, also induced potentiation. 4. 4. Action by phenylhydrazine in the course of oxidation was not selective for insect tissue, because contractions of a frog gastrocnemius preparation and a turtle heart preparation were abolished. 5. 5. The findings do not support the hypothesis that L-glutamic acid decarboxylase inactivates L-glutamate at the insect excitatory neuromuscular junctions.