BACKGROUND: Although the efficacy of morphine in the neuropathic pain state is somewhat controversial, spinally administered morphine reversed the tactile allodynia in our previous animal study. Using a von Frey filament test, we examined the mechanism of action of intrathecal morphine by administration of the opioid receptor antagonist naloxone in a rat model of neuropathic pain induced by nerve ligation injury. METHODS: Male Sprague Dawley rats were prepared with tight ligation of the left lumbar 5th and 6th spinal nerves and a chronic lumbar intrathecal catheter. Intrathecal doses (0.3 and 1 microgram) of morphine were administered to attenuate the allodynic state. Naloxone was administered intrathecally (10 microgram) or intraperitoneally (30 and 150 microgram) in order to investigate the reversal of the antiallodynic effect of morphine. Allodynic thresholds for left hindpaw withdrawal to the von Frey hairs test were assessed and converted to %MPE. RESULTS: A reduced effect of tactile allodynia by intrathecal morphine was produced. Naloxone 10 microgram (IT) and 150 microgram (IP), but not naloxone 30 microgram (IP), reversed the antiallodynic effect of intrathecal morphine (P < 0.05). CONCLUSIONS: The results suggest that the mechanism of tactile antiallodynia induced by intrathecal morphine may include the opioid receptor system at the spinal and supraspinal level in a rat model of nerve ligation injury.