oxytocin and Alcoholic-Intoxication

The effects of acute ethanol administration on the ingestion of NaCl and food were assessed in adult rats subjected to 1-hr drinking and feeding tests 30 min after intraperitoneal administration of ethanol. Ethanol pretreatment did not induce spontaneous NaCl ingestion, but significantly potentiated angiotensin II-stimulated salt appetite, but not water intake, in a dose-dependent manner. Similarly, ethanol pretreatment significantly potentiated neuropeptide Y-stimulated food intake in nonfasted rats, but did not, by itself, cause spontaneous food ingestion. Ethanol pretreatment also significantly blunted pituitary secretion of oxytocin in response to multiple excitatory stimuli. Finally, administration of oxytocin intracerebroventricularly prevented the ethanol-induced potentiation of salt appetite elicited by angiotensin II. In view of our previous findings that central oxytocin secretion inhibits both NaCl and food intake, we propose that ethanol potentiates the ingestion of various solutes in rats, in part, by inhibiting brain-projecting oxytocinergic pathways concurrently with its well-known effects to inhibit pituitary oxytocin secretion.

Topics: Alcoholic Intoxication; Animals; Dose-Response Relationship, Drug; Drinking; Eating; Ethanol; Male; Neural Inhibition; Neuropeptide Y; Oxytocin; Pituitary Gland; Rats; Rats, Sprague-Dawley; Renin-Angiotensin System; Water-Electrolyte Balance