Abstract
Previous studies have established that the antinociceptive effect of morphine was subjected to peptidergic modulation at spinal level. Intrathecal (i.t.) galanin (GAL) potentiated morphine-induced analgesia, whereas i.t. cholecystokinin (CCK) antagonized morphine's hypoalgesic effect. In the present study, we examined the possible interaction between GAL, CCK and clonidine, an α 2 adrenoceptor agonist and potent spinal antinociceptive agent, in the spinal nociceptive flexor reflex. I.t. clonidine dose-dependently depressed the flexor reflex similarly to i.t. morphine However, unlike morphine, the reflex depressive effect of i.t. clonidine was neither potentiated by i.t. GAL nor blocked by i.t. CCK. The present results suggested that the analgesia elicited by activation of spinal α 2 adrenoceptors is not subjected to the modulatory effect of CCK and GAL and therefore may be mediated through different mechanisms than opioids.
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