Spinal δ_2-, but not δ_1-, μ-, or κ-opioid receptors are involved in the tail-flick inhibition induced by β-endorphin from nucleus raphe obscurus in the pentobarbital-anesthetized rat

The antinociception induced by β-endorphin given supraspinally has been previously demonstrated to be mediated by the release of [Met⁵]enkephalin acting on δ-opioid receptors in the spinal cord. The present study was designed to determine what type of opioid receptors in the spinal cord is involved in β-endorphin-induced antinociception in the rat. Antinociception was induced by β-endorphin (0.6 nmol) given into nucleus raphe obscurus and was assessed by the tail-flick test in pentobarbital-anesthesized rats. Naltriben (0.6-6.0 nmol), a selective δ₂-opioid receptor antagonist, given intrathecally dose-dependently attenuated β-endorphin-induced inhibition of the tail-flick response. On the other hand, 7-benzylidene naltrexone (2.1-64.3 nmol), CTOP (d-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr-NH₂, 0.09-2.8 nmol), or nor-binaltorphimine (1.4-40.8 nmol), selective δ_1-, μ-, and κ-opioid receptor antagonists, respectively, did not block β-endorphin-induced antinociception. The results of present study in rats are consistent with previous experiments in mice indicating that spinal δ_2-, but not δ_1-, μ- or κ-opioid receptors are involved in β-endorphin-induced inhibition of the tail-flick response.