Aim: The central nucleus of amygdala (CeA) is involved in emotional pain response and descending control of pain. Recent studies indicate that corticotropin-releasing factor (CRF) is involved in amygdaloid modulation of pain and anxiety. CRF binding protein (CRF-BP) is also localized in the amygdala and it reduces action of CRF by binding free CRF. In this study, we determined whether amygdaloid CRF contributes to pain modulation in neuropathy induced by peripheral nerve injury in the rat. Methods: Emotional/affective aspect of pain was assessed by an aversive place-conditioning test. Sensory aspect of pain and its descending modulation was assessed by determining limb withdrawal threshold to mechanical stimulation of the paw. CRF_6-33, an inhibitor of CRF-BP, or CRF_9-41, a non-selective CRF receptor antagonist, was microinjected through a chronic guide cannula to the CeA contralateral to peripheral nerve injury. Results: CRF_6-33 in the CeA attenuated emotional pain-like behavior. The CRF_6-33-induced attenuation of emotional pain-like behavior was associated with a facilitation of the sensory-discriminative aspect of pain as revealed by a decrease of the limb withdrawal threshold. These effects were reversed by CRF_9-41. Conclusion: The results indicate that endogenous CRF in the amygdala, through action involving CRF receptors, may differentially influence emotional and sensory aspects of pain in neuropathy.