BACKGORUND: A nerve ligation injury may produce a pain syndrome including mechanical allodynia. Usually the antiallodynic effect of morphine is diminished in a neuropathic rat model. However, in a previous study, spinal morphine was found to have an antiallodynic effect in a neuropathic rat model. Therefore, the present study was performed to observe the mechanical antiallodynic effects of spinal morphine and R-PiA, and to investigate the relationship between the two. METHODS: Male SD rats were prepared by tightly ligating the left L5 and L6 spinal nerve and by implanting a lumbar intrathecal catheter. in study 1, each of the 5 groups (morphine at 3 or 10mug, adenosine A1 receptor agonist (R-PiA) at 3 or 10mug, or saline) were administered intrathecally to examine changes in the mechanical allodynia threshold. in study 2, selective adenosine A1 receptor antagonist (DPCPX 10mug) was administered to investigate the reversal of the mechanical antiallodynic effect in the 4 treated groups. in study 3, we observed the pretreatment effect of DPCPX 10mug. The mechanical allodynic thresholds for left hindpaw withdrawal to von Frey hairs were assessed and converted to %MPE. RESULTS: in study 1, the mechanical allodynic threshold was significantly increased in a similar pattern by intrathecal morphine (3, 10mug) and R-PiA (3, 10mug) (P<0.05). in study 2, the allodynic threshold of morphine was insignificantly decreased by intrathecal DPCPX pretreatment. The mechanical allodynic threshold of R-PiA 3mug was decreased by intrathecal DPCPX (P<0.05). in study 3, the antiallodynic effect of morphine was not influenced by DPCPX pretreatment. CONCLUSiONS: intrathecal morphine and R-PiA produced the antiallodynic effect. The antiallodynic effect of morphine was slightly decreased by DPCPX 10mug. Therefore, it was suggested that the antiallodynic effect of morphine might be, at least in part, mediated by adenosine in a rat model of spinal nerve ligation.