CHOLECYSTOKININ-A BUT NOT CHOLECYSTOKININ-B RECEPTOR STIMULATION INDUCES ENDOGENOUS OPIOID-DEPENDENT ANTINOCICEPTIVE EFFECTS IN THE HOT PLATE TEST IN MICE

The effects of intracerebroventricular administration of the cholecyst okinin (CCK) analogue, BDNL, and the selective CCK-B agonist, BC 264, were determined using the hot plate test in mice. BDNL (0.2 nmol and 0 .5 nmol) increased the jump and the paw lick latencies. These effects were blocked by the CCK-A antagonist MK-329 (0.02 mg/kg), supporting t he involvement of CCK-A receptors in CCK-induced analgesia. In contras t, the selective CCK-B agonist BC 264 produced, at one dose (2.5 nmol) , a slight decrease in the lick latency that was only antagonized by t he CCK-B antagonist. Naloxone, but not naltrindole, antagonized BDNL-i nduced analgesia. The results suggest that activation of CCK-A recepto rs by BDNL leads to antinociceptive responses indirectly mediated by s timulation of mu-opioid receptors by endogenous enkephalins.