• 1 January 1985
    • journal article
    • research article
    • Vol. 232  (1) , 74-79
Abstract
Opioids applied to supraspinal brain sites may produce their analgesic effects by the activation of different descending pain inhibitory systems. The blockade of the spinal endorphinergic system by intrathecal naloxone on the production of tail-flick inhibition induced by intraventricular .beta.-endorphin and morphine was studied. Intraventricular injection of .beta.-endorphin and morphine produced an inhibition of the tail-flick response to the heat stimulus in rats. Intrathecal injection of naloxone at doses of 0.4-40 .mu.g caused a dose-related blockade of the inhibition of the tail-flick response induced by intraventricular injection of .beta.-endorphin, and a high dose of naloxone (40 .mu.g) completely blocked the tail-flick inhibition induced by intraventricular .beta.-endorphin (16 .mu.g). Intrathecal naloxone (12-120 .mu.g) had only a very weak effect on the tail-flick inhibition induced by intraventricular morphine (40 .mu.g). Intraventricular injection of naloxone at doses of 1.2-12 .mu.g equally antagonized in a dose-dependent manner the tail-flick inhibition induced by intraventricular .beta.-endorphin and morphine. Evidently a spinal naloxone-sensitive endorphinergic system is involved in the production of .beta.-endorphin but not morphine-induced tail-flick inhibition. Intraventricular .beta.-endorphin and morphine may elicit their pharmacological actions via the activation of different descending pain inhibitory systems; descending .epsilon. and .mu. systems for .beta.-endorphin and morphine, respectively, are proposed.