Mechanisms of the effect of Icv IL-1β on oxytocin release in the anesthetized, lactating rat.

Interleukin-1β stimulates the release of many hypothalamic hormones, including oxytocin. Experiments were done to examine the effect of icv IL-1β on circulating oxytocin levels in rats throughout lactation, and to determine if alpha-adrenergic mechanisms and/or prostaglandins were involved as mediators. Blood samples were taken from urethane-anesthetized, nonlactating and lactating rats before and after icv treatment with either IL-1β or PBS-BSA; or icv treatment with IL-1β following pretreatment with either phentolamine or indomethacin. Plasma was assayed using a specific oxytocin radioimmunoassay. Interleukin-1β stimulated oxytocin release in all rats tested resulting in an approx 2- to 2.5-fold increase in plasma hormone levels. Throughout the first half of lactation, oxytocin responsiveness to IL-1β increased. On d 20 of lactation, the plasma oxytocin response to IL-1β was depressed. Adrenergic mechanisms may be involved in this differential effect on oxytocin release in lactation as phentolamine pretreatment attenuated IL-1β-induced oxytocin release in early lactation and reversed the depression in IL-1β-stimulation of oxytocin release observed in late lactation. It is possible that central IL-1β is involved in the weaning process: oxytocin responsiveness to IL-1β increases throughout the first half of lactation when oxytocin demands are high and is depressed in late lactation when weaning is occurring.