Neuropathic pain remains a major complication of various forms of injury to peripheral nerves in humans. Recently, 2 models of peripheral mononeuropathy in the rat have been described which closely resemble the human condition. Bennett and Xie3 described one model induced by the placement of 4 loose ligatures around the entire sciatic nerve; Seltzer et al. have described a second model produced by the placement of a tight ligature around one-third to one-half of the sciatic nerve. It is the purpose of this work to compare the effect of these injuries on the time course and magnitude of hyperalgesia as measured by paw withdrawal latency to a radiant heat stimulus. In addition, to evaluate the hypothesis that neuropathic pain develops as a result of injury-associated discharges, some injuries were induced following anesthesia of the sciatic nerve. Our results show that the partial constriction neuropathy (PCN) described by Bennett and Xie3 develops in a faster time frame than that produced by the tight ligature, or partial transection neuropathy (PTN), described by Seltzer and co-workers. In addition, the PCN shows a reduction in both the duration and magnitude of behavioral hyperalgesia obtained for those animals in which local anesthetic (lidocaine) was applied to the sciatic nerve, while the PTN does not show this sensitivity. The data suggest that injury-related discharge is one important factor contributing to the generation of hyperalgesia in the PCN model. The mechanism(s) responsible for the generation of hyperalgesia in the early stages of the PTN model are not lidocaine-sensitive.(ABSTRACT TRUNCATED AT 250 WORDS)