Deletion of μ-opioid receptor in mice does not affect the minimum alveolar concentration of volatile anaesthetics and nitrous oxide-induced analgesia

Background The role of the endogenous opioid system in the anaesthetic effect of volatile anaesthetics and the analgesic action of nitrous oxide (N 2 O) is unclear. In the current study, we investigated whether the μ-opioid receptor (MOP) is involved in these activities using MOP knockout (MOP-KO) and wild-type (WT) mice. Methods Minimum alveolar concentrations (MACs) for sevoflurane, isoflurane, and halothane, and the sevoflurane MAC-sparing effect of N 2 O were determined in homozygous MOP-KO and WT mice. The analgesic effect of N 2 O and the suppressive effect of naloxone on N 2 O analgesia were assessed in a writhing test and a hot-plate test. Immunohistochemical staining was used to visualize N 2 O-induced c-Fos expression in the lumbar spinal cord. Results There were no significant differences in the MAC values of the three volatile anaesthetics or in the sevoflurane MAC-sparing effect of N 2 O 70% between MOP-KO and WT mice. There was also no significant difference in the analgesic effect of N 2 O 70% or in the level of c-Fos expression induced by N 2 O 70% between the two genotypes. In the writhing test, naloxone significantly attenuated N 2 O analgesia in MOP-KO and WT mice. Conclusions These results suggest that MOP is not required for the anaesthetic action of volatile anaesthetics and the analgesic effect of N 2 O. Opioid receptors other than MOP may mediate the analgesic action of N 2 O.