Lack of sensitization of primary afferent receptors by prostaglandins in a rat model of causalgic chronic pains.

Unilateral entrapment of half of the sciatic nerve in a ligature rapidly produces in rats bilateral hyperalgesia: decreased withdrawal thresholds to von-Frey hair touch and to noxious CO2 laser heat pulses and unilateral hyperpathic responses to a supra-maximal noxious heat pulse. These abnormal pain responses last many months and are very similar to those seen in humans with causalgia. In the present study we determined whether the underlying mechanism involves bilateral sensitization of primary afferent receptors. Since the responses of rats with partial sciatic injury to stimulation of rostral areas (forepaws, muzzle and auricles) were normal, we presume that the hyperalgesia at the contralateral hindpaw could not be due to receptor sensitization, but to rapid central plasticity. Moreover, since indomethacin did not prevent the bilateral hyperalgesia, we conclude that the causalgiform pain disorders seen in the ipsilateral hindpaw did not derive from receptors sensitized by prostaglandins.