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This review will focus on the activity of oxytocin neurons in the supraoptic nucleus (SON) and some factors that regulate their function during parturition and milk ejection in the rat. The level of oxytocin increases in the blood during parturition following a regression of the corpus luteum. The increase in oxytocin secretion is presumably a consequence of releasing the oxytocin neurons from restraining inhibitory influences of endogenous opioids-, nitric oxide-, and GABA-containing neurons following declining blood levels of progesterone on the one hand and increasing levels of estrogen on the other during late pregnancy. However, the principal stimulus for the increased oxytocin release is believed to originate, at least in part, from mechanical stimulation to the uterine cervix by fetuses near term, the resultant uterine contractile activity, and the fetal expulsion reflex. Hence, the contractile activity of the uterus acts through positive feedback mechanisms during parturition to stimulate oxytocin neurons as well, and this further increases the secretion of oxytocin. During suckling in lactating rats, somatosensory stimuli from the pups induce intermittent synchronized burst firing of oxytocin neurons, resulting in pulsatile increases in blood oxytocin concentrations to cause milk ejection. The oxytocin neurons appear to have an intrinsic capability to fire in a bursting fashion as determined by observation of this phenomenon in brain slice or tissue culture preparations. The release of oxytocin within the microenvironment of the SON and paraventricular nucleus coupled with morphological reorganization in these nuclei play important roles in the bursting activity of each oxytocin neuron and synchronization in vivo. However, the mechanism responsible for the synchronization of electrical activity in oxytocin neurons in the four discrete hypothalamic nuclei remains an interesting unanswered question.

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