Spinal β-endorphin analgesia involves an interaction with local monoaminergic systems

Abstract

β-Endorphin administered intrathecally (i.t.) in rats produced a dose-dependent elevation in tail-flick latency. Naltrexone administered i.t. as a pretreatment reversed the spinal antinociceptive action of β-endorphin, suggesting that the opioid interacts directly with spinal opiate receptors. Spinal administration of the α 1-adrenoceptor antagonist WB-4101 failed to alter the analgesic effects of the opioid, whereas the α 2-adrenoceptor antagonist yohimbine completely blocked β-endorphin-induced elevations intail-flick latency. Thus, there is an apparent specificity for the α 2-adrenoceptor to mediate the spinal action of β-endorphin. The 5-HT 1 and 5-HT 3 receptor antagonists (spiroxatrine and ICS 205–930, respectively) also reversed the analgesic effects of the opioid, while the 5-HT 2 receptor antagonist ritanserin only partially blocked β-endorphin-induced elevations in tail-flick latency. The present results suggest that β-endorphin produces analgesia at the spinal level via an opiate receptor-mediated interaction with spinal monoaminergic nerve terminals.