Abstract
The effects of RB 101 {N-[(R,S)-2-benzyl-3[(S)(2-amino-4-methylthio)butyl dithio]-1-oxo-propyl]-L-phenylalanine benzyl ester}, a complete inhibitor of enkephalin-degrading enzymes and CI 988, a selective antagonist of the cholecystokinin (CCK)-B receptors, on the flexor reflex in decerebrate, spinalized, unanaesthetized rats were assessed. Intravenous RB 101 induced a dose-dependent depression of the flexor reflex with a threshold dose of 20 mg/kg and an ED 50 of 25.3 mg/kg. Subcutaneous CI 988 at 1 mg/kg, which by itself did not influence the flexor reflex, strongly enhanced the reflex depressive effect of RB 101. The dose-response curve for RB 101 was shifted to the left and the duration of reflex depression was significantly prolonged. The results confirmed and extended previous behavioural data indicating that blockade of CCK-B receptors potentiated antinociception elicited by endogenous opioids protected from enzymatic degradation. Furthermore, the spinal cord is an important site of interaction between the endogenous opioid and CCK systems.
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