Unilateral dorsal rhizotomy of brachial plexus nerves (C5-Th1) performed under general anesthesia is known to induce self-mutilation in rats. The aim of this study was to determine the effect of different anesthetic agents, and of pre-rhizotomy nociceptive stimulation on the appearance of self-mutilation. Self-mutialtion appeared in 78 % of animals after rhizotomy had been performed under pentobarbital anesthesia. When ketamine was used as the general anesthetic, self-mutilation was almost suppressed (13 %) and consisted of superficial erosions. Mechanical nociceptive stimulation, when applied just before the induction of ketamine anesthesia and subsequent rhizotomy, provoked self-mutilation in 91 % of rats. Furthermore, a serious type of self-mutilation consisting of total amputation of the distal part of the forepaw was present in 28 % of all self-mutilating animals after previous nociceptive stimulation. In terms of self-mutilation, these results suggest 1) the crucial role of anesthesia, especially that which involved NMDA receptors (ketamine), and 2) the need of an additional factor to chronic deafferentation, formed either by activity of nociceptive pathways just before rhizotomy (nociceptive stimulation preceding ketamine anesthesia) or by injury discharges (pentobarbital anesthesia).
Unilateral deafferentation induced by transection of the C4-C8 dorsal roots of spinal cord, followed by a complex of abnormal self-mutilating behavior, is interpreted as an animal model of chronic nociception. The objective of our study was to test the differences in tail-flick latency between intact control and unilaterally deafferented animals and to assess the changes in their acute nociceptive sensation. The initial hypothesis was that deafferentation-induced painful sensation might cause stress-induced analgesia that should be manifested as prolonged tail-flick latency. The experiment was carried out on 11 male and 10 female adult Wistar rats. The tail-flick latency was repeatedly measured over a period of 10 consecutive weeks both in the preoperative baseline period and following multiple cervical dorsal rhizotomy. Contrary to our hypothesis, unilateral deafferentation was followed by a significant shortening of the tail-flick latency both in males and females. In deafferented animals, compared to the controls, variations of tail-flick latency were reduced. In individual animals after deafferentation, concurrent dynamic changes were observed in self-mutilating behavior, in a loss and regaining of body weight, and in tail-flick latency. Our data suggest that changes in tail-flick latency may be interpreted in terms of central sensitization and that tail-flick latency might be considered as a useful marker of chronic nociception.