The prevailing view is that supraspinal μ opioid-mediated antinociception in mice is mediated via the μ1 subtype. The purpose of the present study was to determine if the highly μ-selective compound etonitazene could produce supraspinal (intracerebroventricular; i.c.v.) antinociception in CXBK mice, which are deficient in brain μ1, but not μ2, opioid receptors. CXBK or normal Crl:CD-1 ®(ICR)BR mice were administered graded doses of etonitazene i.c.v. and 15 min later antinociception was assessed by a standard radiant-heat or 55°C water tail-flick test. Etonitazene produced dose-related antinociception that was blocked by naloxone and by β-FNA (demonstrating a μ opioid mechanism), but not by either ICI-174,864 or naltrindole (demonstrating the lack of involvement of δ opioid receptors). These findings suggest that μ2 opioid receptors are important contributors to opioid-induced supraspinal antinociception in mice.
- CXBK mice
- opioid receptor subtypes
- opioid μ receptors
- μ/μ subtypes
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Pharmacology, Toxicology and Pharmaceutics(all)