CONDUCTION BLOCK OF TERMINAL SOMATIC MOTOR FIBERS IN TICK PARALYSIS

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Abstract
In the perfused anterior tibial muscle of the tick-paralyzed dog acetylcholine in excess of the control value is not liberated on stimulation of the peroneal nerve; in the normal muscle 7 μμg of acetylcholine is liberated per nerve volley. The paralysis is evidently not due to defective synthesis of acetylcholine because acetylcholine is liberated in control and high-potassium perfusates, the choline acetylase activity and the acetylcholine content of lumbar ventral roots and peroneal nerves do not differ from that in normal dogs, and the tick-paralyzed muscle differs from that in the hemicholinium-treated animal in its response to a train of nerve pulses after previous tetanization. As somatic motor nerve fibers in the paralyzed dog have previously been shown to conduct a nerve impulse and the factors required for acetylcholine release at the nerve terminal apparently are not absent in the paralyzed animal, the mechanism of the paralysis is probably due to an inability of the nerve impulse to traverse the terminal presynaptic fibers. The 'lesion' evidently extends to the end of the presynaptic fiber, i.e. more distally than in botulism, because direct stimulation of the tick-paralyzed muscle fails to liberate acetylcholine.