In parallel, the studies on rodent models of neuropathic pain reveal that the expression of the excitatory bradykinin receptors is enhanced in the CNS and PNS in painful neuropathy states [143]; therefore, once the its release is elevated, dynorphin can exert pronounced antiopioid effects through binding to bradykinin receptors, and the effects may be counteracted with B1 and B2 antagonists to alleviate the hypersensitivity [27,47]. The gene discussed is PDYN; the disease is neuropathy.