Journal
ADDICTION BIOLOGY
Volume 18, Issue 4, Pages 614-622Publisher
WILEY
DOI: 10.1111/j.1369-1600.2011.00354.x
Keywords
Fentanyl; mouse; neuropathic pain; opioid tolerance; -opioid receptor; spinal cord
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Funding
- NIDA NIH HHS [R37 DA008863, R01 DA008863, K05 DA019521] Funding Source: Medline
- NINDS NIH HHS [R01 NS026880] Funding Source: Medline
- Grants-in-Aid for Scientific Research [21600009, 23592299] Funding Source: KAKEN
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In the present study, we investigated the possible development of tolerance to the antihyperalgesic effect of mu-opioid receptor (MOR) agonists under a neuropathic pain-like state. Repeated treatment with fentanyl, but not morphine or oxycodone, produced a rapid development of tolerance to its antihyperalgesic effect in mice with sciatic nerve ligation. Like the behavioral study, G-protein activation induced by fentanyl was significantly reduced in membranes obtained from the spinal cord of nerve-ligated mice with in vivo repeated injection of fentanyl. In -endorphin-knockout mice with nerve ligation, developed tolerance to the antihyperalgesic effect of fentanyl was abolished, and reduced G-protein activation by fentanyl after nerve ligation with fentanyl was reversed to the normal level. The present findings indicate that released -endorphin within the spinal cord may be implicated in the rapid development of tolerance to fentanyl under a neuropathic pain-like state.
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