, Volume 24, Issue 2, pp 297-299
Date: 17 Feb 2010

Involvement of the κ-opioid receptor in nitrous oxide-induced analgesia in mice

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Nitrous oxide (N2O)-induced analgesia is thought to be mediated by endogenous opioids. We previously showed that the μ-opioid receptor is not required for the analgesic action of N2O in mice using a gene knockout approach. In this study, we examined the effect of κ- (KOP)- or δ-opioid receptor (DOP)-selective antagonists on N2O-induced analgesia. The analgesic effect of N2O was evaluated using a writhing test. Male C57BL/6 mice aged 7–8 weeks were assigned to control, N2O, KOP agonist, and DOP agonist groups. According to the group assignment, mice were pretreated with a KOP antagonist, nor-binaltorphimine (nor-BNI), a DOP antagonist, naltrindole hydrochloride (NTI), a KOP agonist U50488, and a DOP agonist SNC80. Mice in the control, KOP agonist, and DOP agonist groups were exposed to 25% oxygen/75% nitrogen for 30 min, and mice in the N2O group were exposed to 25% oxygen/75% N2O for 30 min. Nor-BNI [10 mg kg–1, subcutaneously (s.c.)] significantly suppressed the analgesic effect of N2O and U50488. In contrast, NTI (10 mg kg–1 s.c.) did not significantly affect the analgesic action of N2O, but almost completely inhibited the analgesic effect of SNC80. These results suggest that KOP plays an important role in the analgesic effect of N2O in mice.