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Several neuroscientists have linked opioid abuse in the presence of pain to the mesolimbic pathways, especially dopaminergic tone.40–42 One potential mechanism for hyperalgesia involves chronic morphine reducing the rewarding and nociceptive properties of opioids due to decreased DA release in the NAc43 and increased tumor necrosis factor-alpha levels in the NAc.44 Importantly, l-tetrahydropalmatine alleviates mechanical hyperalgesia in chronic inflammatory and neuropathic pain models in mice, an effect blocked by a DA D1 receptor antagonist.44 Dias et al showed that increasing DA in the NAc with the DA reuptake inhibitor GBR12909 blocked prostaglandin E2-induced acute hyperalgesia, an effect prevented by a DA D2 receptor antagonist but not by a D1 receptor antagonist.45 Hoshino et al demonstrated the antihyperalgesic effects of intrathecal bupropion, a DA, and noradrenaline reuptake inhibitor, in a rat model of neuropathic pain.46 These findings highlight the significant contribution of the descending inhibitory pathways, involving noradrenaline and DA, to the maintenance of neuropathic pain
