Serotoninergic Mechanisms of Beta-Endorphin- and Clonidine-Induced Analgesia in Rats

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Abstract
.beta.-Endorphin and clonidine had statistically significant analgesic activity (increase in latency to hind-paw lick in hot plate test) in rats. The pain inhibition induced by .beta.-endorphin and clonidine could be antagonized by prior treatment of animals with naloxone (a narcotic antagonist) or depletors of central serotonin pathways, i.e., 5,6-dihydroxytryptamine, 5,7-dihydroxytryptamine and p-chlorophenylalanine. Naloxone, 5,6-dihydroxytryptamine, 5,7-dihydroxytryptamine and p-chlorophenylalanine do not effect latency to hind-paw lick. The data indicate that serotoninergic activity in the brain plays a role in the elaboration or modulation of .beta.-endorphin and clonidine analgesia in rats.