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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Base and stress levels of corticosterone were assessed at 4-h intervals over a 24-h period in male and female rats at age 18, 22, and 26 days. A significant periodicity in base levels of corticosterone is present at 22 days of age; however, a rhythm in stress values does not appear until age 26 days. At age 26 days the pattern of the circadian periodicity in both base and stress concentrations of corticosterone resembles that of the mature rhythm.

Implantation of crystalline cortisol acetate in the medial basal hypothalamus (MBH), apart from inhibiting pituitary adrenal responses, had a profound suppressive effect on the reproductive system of the immature (30-day-old) rat autopsied 3 weeks after implantation. The development of testes, seminal vesicles, and prostates through the period of puberty was effectively prevented, and spermiogenesis was absent. In the female, estrous cycling was absent, ovarian and uterine development was prevented, and ovulation did not occur. Adrenalectomy in nonimplanted animals had none of these effects. ACTH in doses producing slight to marked adrenal hypertrophy did not influence the changes produced by cortisol implants. It is concluded that cortisol has a direct suppressive effect on gonadottopin secretion at the hypothalamo-pituitary level.