While cannabinoid receptor agonists reduce the abnormal pain sensations associated with animal models of neuropathic pain states they also produce CB 1 receptor mediated side effects. Recently, a number of arachidonic acid–amino acid conjugates, including N-arachidonyl-glycine (NAGly), have been identified which are structurally related to the endocannabinoid arachidonyl ethanolamide (anandamide). In the present study we examined the effect of NAGly in a rat model of neuropathic pain. Intrathecal administration of NAGly (700nmol) and the pan-cannabinoid receptor agonist HU-210 (30nmol) reduced the mechanical allodynia induced by partial ligation of the sciatic nerve. The NAGly induced anti-allodynia was dose dependent and, unlike HU-210, was unaffected by the cannabinoid CB 1 and CB 2 receptor antagonists, AM251 and SR144528 (30nmol). The NAGly degradation products, arachidonic acid and glycine (700nmol), did not reduce allodynia. HU-210, but not NAGly produced a reduction in rotarod latency. These findings suggest that NAGly may provide a novel analgesic approach to alleviate neuropathic pain.