2016
DOI: 10.1073/pnas.1602070113
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Abstract: Opioid use for pain management has dramatically increased, with little assessment of potential pathophysiological consequences for the primary pain condition. Here, a short course of morphine, starting 10 d after injury in male rats, paradoxically and remarkably doubled the duration of chronic constriction injury (CCI)-allodynia, months after morphine ceased. No such effect of opioids on neuropathic pain has previously been reported. Using pharmacologic and genetic approaches, we discovered that the initiation… Show more

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Cited by 300 publications
(312 citation statements)
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“…This toxicity may commence after brief exposure and leave a vulnerability to increased pain responses that may be of indefinite duration. 20 Other long-term opioid toxicities include depression, sleep interference, hypogonadism, prolonged disability and delayed return to work.…”
Section: Why Opioids Are No Longer First Linementioning
confidence: 99%
“…This toxicity may commence after brief exposure and leave a vulnerability to increased pain responses that may be of indefinite duration. 20 Other long-term opioid toxicities include depression, sleep interference, hypogonadism, prolonged disability and delayed return to work.…”
Section: Why Opioids Are No Longer First Linementioning
confidence: 99%
“…Recent data has shown that prolonged treatment with morphine doubled the duration of pain associate with nerve injury independent of opioidreceptor selectivity. [21] Morphine-mediated persistence of pain was attenuated following co-administration with the IL-1 receptor antagonist (IL-1ra). [21] Prolonged morphine use can activate glial toll-like receptors such as the toll-like receptor 4 (TLR4) which following priming ensures neurotoxicity, immune mediated amplification of nociceptive signaling in the spinal cord.…”
Section: Wwwnnjournalnetmentioning
confidence: 99%
“…[21] Morphine-mediated persistence of pain was attenuated following co-administration with the IL-1 receptor antagonist (IL-1ra). [21] Prolonged morphine use can activate glial toll-like receptors such as the toll-like receptor 4 (TLR4) which following priming ensures neurotoxicity, immune mediated amplification of nociceptive signaling in the spinal cord. [5,[21][22][23] Evidence has also shown that morphine can directly compromise opioid-induced analgesia by promoting proinflammation via a TLR4 dependent mechanism and can potentiate mechanical allodynia.…”
Section: Wwwnnjournalnetmentioning
confidence: 99%
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