Differential mechanisms mediating descending pain controls for antinociception induced by supraspinally administered endomorphin-1 and endomorphin-2 in the mouse.

摘要: We have previously demonstrated that both endomorphin-1 and endomorphin-2 produce their antinociception by the stimulation of μ-opioid receptors. However, induced contains an additional component, which is mediated release dynorphin A (1-17) acting on κ-opioid These studies were done to determine whether given supraspinally was activation different descending pain control pathways in mouse. Specific receptor antagonists or antisera against endogenous opioid peptides injected intrathecally block receptors bind released peptides, then administered i.c.v. activate systems antinociception. The tail-flick response used as antinociceptive test. blockade α2-adrenoceptors 5-hydroxytryptamine spinal cord i.t. injection yohimbine methysergide, respectively, inhibited i.c.v.-administered endomorphin-2. pretreatment with δ2-opioid antagonist naltriben nor-binaltorphimine, but not antagonistd-Phe-Cys-Tyr-d-Try-Orn-Thr-Pen-Thr-NH2or δ1-opioid 7-benzylidene naltrexamine. Intrathecal antiserum Met-enkephalin attenuated endomorphin-2, endomorphin-1. Furthermore, also Leu-enkephalin β-endorphin did inhibit endomorphin-1- endomorphin-2-induced results indicate that, like other μ-receptor agonists, morphine, [d-Ala2, N -Me-Phe4, Gly5-ol]-enkephalin, activating spinipetal noradrenergic serotonergic for producing components, are δ2- κ-receptors, cord.