The function of motor nerves innervating slow tonic skeletal muscle in hens with delayed neuropathy induced by tri-o-tolyl phosphate

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Abstract
The reduction of neurogenic posttetanic potentiation in the slow twitch, soleus muscle is an index of impaired motor nerve function in cats with organophosphate-induced neuropathy. We have applied the measurement of posttetanic potentiation to study the functional state of the slow, tonic, plantaris muscle and its motor innervation in adult White Leghorn hens with tri-o-tolyl phosphate (TOTP)-induced neuropathy. At suitable intervals following single oral doses of vehicle or TOTP (500 mg/kg), nerve conduction velocity and posttetanic potentiation were measured in anesthetized hens. Conduction in the sciatic nerve was not altered by TOTP. The plantaris muscle of birds treated with vehicle (peanut oil) either failed to contract or responded to nerve stimulation at 0.4 Hz with very small twitches. Following nerve stimulation at frequencies inducing tetanus (50–140 Hz), the muscles responded with large, slow twitches that gradually decayed in amplitude. The area under the curve formed by the amplitude of these twitches over time (posttetanic potentiation) was directly proportional to the frequency and duration of nerve stimulation. In hens at 1, 2, and 4 weeks following treatment with TOTP, the average amount of posttetanic potentiation was reduced concomitantly with the development of ataxia, paralysis, and pathological changes in the peripheral nerves. This difference between vehicle- and TOTP-treated hens was not significant, owing to large interbird variations. Since TOTP-treated hens showed greater disturbances in gait following moderate exercise, the fatigue of posttetanic potentiation with periodic neuronal stimulation was measured. In vehicle-treated birds, the posttetanic potentiation remained constant or increased slightly over the 2-h test period; whereas, in the TOTP-treated birds, there was a gradual and variable decrease in posttetanic potentiation, though this could not be correlated with the severity of the ataxia. In contrast with the cat, reduction of posttetanic potentiation in the hen was not a reliable index of the development of delayed neurotoxicity caused by TOTP.