کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2554345 | 1124964 | 2007 | 5 صفحه PDF | دانلود رایگان |
Intracerebroventricular (i.c.v.) administration of the neutral endopeptidase 24.11-inhibitor phosphoramidon evoked a dose-dependent antinociceptive effect in the mouse acetic acid abdominal constriction test. The present study was conducted to identify the opioid receptor subtype(s) that mediate phosphoramidon antinociception in this paradigm. Mice were pretreated with different opioid antagonists prior to being challenged with phosphoramidon, i.c.v., the μ-opioid agonist sufentanil, s.c., or the κ-opioid agonist U-50,488H, s.c. Naltrexone significantly attenuated phosphoramidon-induced antinociception at an i.c.v. dose that also blocked both sufentanil and U-50,488H. The μ-opioid antagonist β-funaltrexamine (β-FNA) blocked phosphoramidon and sufentanil at an i.c.v. dose that did not block U-50,488H. The κ-opioid antagonist nor-binaltorphimine (nor-BNI) produced dose-related effects. A low dose (10 μg) of nor-BNI had no effect on either phosphoramidon or sufentanil but did reduce U-50,488H antinociception. A higher dose (30 μg) of nor-BNI blocked phosphoramidon, sufentanil, and U-50,488H, suggesting a loss of κ-opioid receptor selectivity at this dose. These findings suggest that μ- but not κ-opioid receptors mediate phosphoramidon-induced antinociception in the abdominal constriction test.
Journal: Life Sciences - Volume 80, Issue 19, 17 April 2007, Pages 1816–1820