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The ORL1 receptor (opioid receptor-like 1) and its endogenous ligand, nociceptin, are involved in nociperception. We have studied, in a deafferented animal model, the modification of medullar [(3)H]nociceptin binding site density. A rhizotomy was carried out in rats at the cervicothoracic level, and the dorsal afferent fibers from C5 to T1 were lesioned. Seven days after surgery, animals were sacrificed, and the binding of [(3)H]nociceptin (2 nM) was then performed on spinal cord sections. An autoradiographic analysis revealed a significant reduction (-18%) of [(3)H]nociceptin binding site density in the dorsal horn ipsilateral to the deafferentation compared with the contralateral side of the lesion. In the ventral horn, no significant difference (-5%) of binding was observed in the ipsilateral side of the deafferentation compared with the contralateral side. Thus, [(3)H]nociceptin binding sites appear to be located mainly on either interneurons or deutoneurons of the spinal cord, because the bulk of the labeling is spared by the lesion. However, the significant reduction of labeling that occurs on the dorsal part of the ipsilateral side to the lesion indicates that [(3)H]nociceptin binding sites are also present on these dorsal afferent fibers., (Copyright 2002 Wiley-Liss, Inc.)

When placed on a hot plate, rats with 5 consecutive dorsal root sections, present long licking-latencies of the posterior limbs, sign of a generalised hypoalgesia. To determine if this hypoalgesia is the result of the deafferentation or of the extent of the anterior limb automutilation performed by such deafferented rats, the licking-latency was measured in two groups of deafferented rats. In one of these groups all the rats performed automutilation, in the other a daily injection of amoxicillin resulted in an important reduction of the autotomic behavior. In both groups the licking-latency was twice its value in non-deafferented animals (order of 14 s in place of 7 s). Thus, hypoalgesia is the consequence of the deafferentation and not of the connected automutilation extent. To explain these results it is proposed that this hypoalgesia results from the algic sensitivity decrease observed in a normally afferented area when a painful sensation is felt in an other territory, the deafferented area in this case.