Milk ejection reflex

Abstract: Studies in animals indicate that various types of stressful stimuli can depress lactation, but there is much less information in humans. Experimental studies in breastfeeding women have shown that acute physical and mental stress can impair the milk ejection reflex by reducing the release of oxytocin during a feed. If this occurs repeatedly, it could reduce milk production by preventing full emptying of the breast at each feed. Prospective observational studies indicate that both maternal and fetal stress during labor and delivery (e.g., urgent Cesarean sections or long duration of labor in vaginal deliveries) are associated with delayed onset of lactation. The effects of chronic emotional stress on lactation are not known. Mothers who experience high levels of stress during and after childbirth should receive additional lactation guidance during the first week or two postpartum.

Abstract: 1. Antidromically identified supraoptic (SO) units were recorded in lactating rats anaesthetized with urethane (1·1 g/kg), and their activity was studied during milk ejection evoked by the suckling of the young. Fifty-eight SO units were recorded through 174 milk ejections. Each milk ejection was the result of a neurohypophysial release of an oxytocin pulse of 0·5-1·5 m-u. 2. Fifty-five of the SO units displayed background activity and three were silent. The firing rates ranged from 0 to 15·4 spikes/sec, the distribution was exponential with 26% of the units firing at < 1 spike/sec. Sixteen (28%) of the SO units displayed a phasic pattern of activity characterized by periods of activity (6-132 sec) and silence (4-71 sec). 3. Twenty-five of the non-phasic units displayed a large and stereotyped acceleration in spike activity some 10·5-17·4 sec before the rise in intramammary pressure at milk ejection. Units accelerated to rates between 9-66 spikes/sec, an increase of about thirtyfold (median) on background activity. The response was brief (0·9-4·7 sec) and was followed by a period of after-inhibition. 4. It was concluded from studies of double recordings and observations of multi-unit activity that all the responsive units were synchronously activated. The mean latency of 13·3 sec between the onset of the neurosecretory response and milk ejection was similar to that observed following the experimental release of endogenous oxytocin by electrical stimulation of the neurohypophysis (50 pulses/sec for 2-4 sec). 5. Four of the phasically active units were correlated with the oxytocin release for milk ejection. Three of these units displayed a burst of activity superimposed on the terminal portion of an active phase, some 10·2-14·7 sec before milk ejection. The fourth unit, recorded in conjunction with a responsive non-phasic unit, consistently switched from silence to activity coincident with the onset of the SO activation. 6. The remaining SO units and a further ten units that were not antidromically activated by neurohypophysial stimulation displayed no change in activity during either the period of neurosecretory activation or the period of after-inhibition. 7. This activation of the SO neurones, in the formulation of oxytocin release and milk ejection, is the same as that we have previously observed in recordings from the paraventricular (PV) region, and the proportion of neurones displaying the response is similar: 48% in the SO nuclei, 58% in the PV nuclei. We conclude, since the SO nuclei contain 80% of the neurosecretory cells that project to the neurohypophysis, that the SO nuclei are as important, if not more so, than the PV nuclei in the control of oxytocin release.

Abstract: The oxytocin and prolactin responses to suckling were measured in 10 women in early (n = 5) and established lactation (n = 5). Oxytocin was released in a pulsatile manner during suckling in all women, but the response was not related to milk volume, prolactin response, or parity of the mother. In all 10 women plasma oxytocin concentrations increased three to 10 minutes before suckling began. In five women this occurred in response to the baby crying, in three it coincided with the baby becoming restless in expectation of the feed, while in two it corresponded with the mother preparing for the feed. There was no prolactin response to stimuli other than stimulation of the nipple associated with suckling. These results clearly indicate that the milk ejection reflex, with release of oxytocin, occurs in most women before the tactile stimulus of suckling. A second release of oxytocin follows in response to the suckling stimulus itself. Thus it is important that care is taken to protect breast feeding mothers from stress not only during suckling but also immediately before nursing, when conditioned releases of oxytocin will occur.