Evidence for the Neuropeptide Cholecystokinin as an Antagonist of Opiate Analgesia

TLDR

The endogenous neuropeptide cholecystokinin, when administered systemically or perispinally, potently antagonizes opiate analgesia produced by foot shock and morphine. Nonopiate foot‑shock analgesia is not reduced by cholecystokinin, which acts at the spinal cord and appears to serve as a specific opiate antagonist in analgesia‑mediating systems, potentially explaining its role in suppressing food intake.

Abstract

The endogenous neuropeptide cholecystokinin, when administered systemically or perispinally, potently antagonizes opiate analgesia produced by foot shock and morphine. Nonopiate foot-shock analgesia is not reduced by this neuropeptide. The spinal cord appears to be a critical site of cholecystokinin action. These experiments suggest a physiological role for cholecystokinin as a specific opiate antagonist in analgesia-mediating systems. A similar mode of action may explain other behavioral effects of cholecystokinin, such as suppression of food intake.