Naloxone potentiation of effects of cholecystokinin and lithium chloride on oxytocin secretion, gastric motility and feeding.

Neurohypophyseal secretion of oxytocin (OT) in response to dehydration, hypovolemia, restraint, and parturition in rats is known to be potentiated by the opioid antagonist naloxone. The present studies demonstrated that stimulation of OT secretion by systemic injections of cholecystokinin (CCK) and lithium chloride (LiCl) likewise are potentiated by naloxone pretreatment. Moreover, the inhibitory effects of CCK and LiCl on gastric motility and feeding similarly were enhanced by naloxone. Because neurohypophyseal hormone secretion and inhibition of gastric motility are known to be mediated by oxytocinergic neurons projecting from the paraventricular nucleus of the hypothalamus, this parallel potentiation by naloxone of CCK- and LiCl-induced effects on OT secretion, gastric motility, and food intake suggests that one of the pathways involved in the central control of feeding behavior also may be oxytocinergic. These findings therefore provide evidence in support of an important role of endogenous opioid peptides in regulating OT secretion in a diffuse neuronal system that mediates an integrated neuroendocrine, autonomic, and behavioral response to CCK, LiCl, and perhaps other treatments that similarly affect ingestive behavior in rats.