Sensory nerves and inflammation: Evidence for the release of a neurogenic permeability factor by Tityustoxin

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Abstract
Venom of the scorpion Tityus serrulatus and its active principle tityustoxin (TsTX), kept in contact with the peripheral cut end of the sciatic or saphenous nerve of the rat, induced inflammatory reactions in the areas supplied by the nerves. The reactions include increased vascular permeability and edema formation below the tibio-tarsal articulation, and were similar to those evoked by electrical antidromic stimulation of these nerves. When electrical stimulation of the peripheral nerve ending preceded its contact with the toxin or, conversely, when the application of electrical pulses closely followed contact with TsTX, no marked increase in the vascular permeability and edematous responses, subsequent to the 2nd stimulation, was observed. Anti-histamine and anti-serotonin drugs, as well as substances capable of blocking synthesis of prostaglandins or activation of the kinin system, and also atropine, were ineffective in reducing the responses to TsTX or electrical stimuli. Since the responses were evoked at a distance in the areas supplied by the nerves, they must be chemically mediated. TsTX and electrical antidromic stimuli affect sensory nerves inducing the release of a permeability-increasing factor, which is responsible for the observed reactions. This factor can be depleted from storage sites by prolonged stimulation of the nerves, is not inhibited by antagonists of known mediators of inflammatory reactions and most probably originates in sensory fibers.