Hypothalamic paraventricular nucleus stimulation-induced gastric acid secretion and bradycardia suppressed by oxytocin antagonist.

Unilateral microstimulation of the medial parvocellular division of the hypothalamic paraventricular nucleus (PVNmp) elicits significant increases in gastric acid secretion and bradycardia. An injection of 25 picomoles of the oxytocin antagonist dET2Tyr(Et)Orn8 Vasotocin (ETOV), suspended in 5 nanoliters of artificial of cerebrospinal fluid (CSF), into the dorsal motor nucleus of the vagus (DMN) immediately preceding microstimulation of the PVNmp suppresses this change in gastric acid secretion and heart rate. The injection of an equal volume (5 nanoliters) of artificial CSF vehicle solution into this region of the DMN, prior to PVNmp microstimulation, has no effect on either the subsequent stimulation-evoked changes in acid secretion or cardiac activity. This suppression of PVNmp stimulation-evoked changes in gastric acid levels and heart rate by the presence of the oxytocin antagonist, ETOV, within the DMN supports the hypothesis that oxytocin may be a neurotransmitter used for descending communication from the PVNmp to neurons within the DMN that regulates these two functions.