Oxytocin secretion from the posterior pituitary gland is required to contract the uterus for birth and the milk ducts for lactation. Prolactin (PRL) is important for maternal adaptations during pregnancy and lactation. In non-pregnant rats, intracerebroventricular (ICV) ovine PRL (oPRL) administration profoundly decreases the firing rate of oxytocin neurons (1). We hypothesized that prolactin inhibition of oxytocin neurons would be reduced at the end of pregnancy and during lactation to permit the increase in oxytocin neuron activity evident during birth and lactation. Using in vivo single-unit electrophysiology, the firing rate of oxytocin neurons were recorded from the supraoptic nucleus of urethane-anaesthetized non-pregnant, pregnant and lactating rats. ICV oPRL (1 and 2 µg/µl) was administered and changes in firing rate of oxytocin neurons were calculated over 5 min pre- and post-oPRL. In non-pregnant and pregnant rats ICV oPRL inhibited the firing rate of oxytocin neurons; this inhibition was evident even in late-pregnant rats (gestation day 18- 22).  During lactation, ~20% of oxytocin neurons were clearly excited (>1 spike/s increase in firing rate) by ICV oPRL. The mechanism behind this prolactin-mediated increase in oxytocin cell firing and the subsequent physiological consequence for lactation is yet to be determined.