The pituitary-adrenal system plays an important role in the initiation and maintenance of lactation in rats, with the suckling stimulus itself inducing the release of ACTH. The recent finding of a reduced plasma corticosterone response to a variety of noxious stimuli during lactation led us to further investigate the activity of this system in lactating (L) rats, compared with post-parturient non-lactating ontrols (NL). Plasma and adrenal corticosterone and plasma ACTH were measured, the latter with a mouse bioassay. Over a 24 h period (12 L:12 D), basal concentrations of plasma corticosterone were elevated in L females, only at those times when the NL basal concentrations were at the trough in the diurnal cycle. At all times, the plasma corticosterone increase 15 min after ether was significantly lower (by a mean of 55 %) in L rats than in NL rats. The elevations in plasma corticosterone after ether were higher for all rats during the day. The night-day difference in response to ether was greater in L rats than in NL rats. Although morning basal levels were not significantly elevated in L females deprived of their litters for 24 h, in these females, as in continually lactating rats, stress concentrations of plasma ACTH (2–4 min after ether) were one third that of the NL controls. Finally, after dexamethasone treatment, the corticosterone output to exogenous ACTH was lower in the plasma and higher in the adrenal in L rats. Thus, pituitary-adrenal activity is altered in a variety of ways during lactation.

In response to ether or electric shock, plasma corticosterone concentrations in weanling and adult rats rose to equivalent levels by 15 min, but then diverged, with the weanlings showing a later peak and a slower return to resting levels. An interpretation of this effect, in terms of an immature feedback mechanism in weanling rats, was supported by an experiment in which pretreatment with peripherally injected dexamethasone completely blocked a plasma corticosterone increase, in response to an ether and blood sampling stress in adults, but only partially reduced this response in weanlings. The failure of basal hypothalamic implants of corticoids to differentiate between ages in their ability to inhibit this stress response supported the suggestion of extra-hypothalamic inhibitory systems as the loci of the deficit in weanlings.

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