Activity of the Pituitary-Adrenal System in Rat Fetuses Subjected to Encephalectomy in Early or Late Stages of Pregnancy

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Abstract
The corticostimulating activity of the fetal rat hypophysis was studied on day 21, in fetuses deprived of their hypothalami by total removal of the brain (encephalectomy) in early (day 16) or late (day 19) stages of gestation. On day 19, the fetal manipulation was performed either on intact or adrenalectomized dams. The data show that: (1) Compared to controls, encephalectomy does not alter pituitary ACTH content in fetuses of intact mothers but that pituitary ACTH content does not significantly increase in encephalectomized fetuses of adrenalectomized mothers whereas it does in the littermate control fetuses. (2) Compared to controls, circulating ACTH levels are reduced by encephalectomy on both day 16 and day 19; an increase in ACTH levels occurs in both fetal groups in response to maternal adrenalectomy. Decapitation removes this fetal source of ACTH. (3) Adrenal glands are not as much atrophied by encephalectomy as by decapitation on day 16, whereas adrenal weight is decreased to the same extent by encephalectomy and by decapitation on day 19. However, the marked increase in circulating ACTH in both control and encephalectomized fetuses caused by maternal adrenalectomy is probably the cause of the significant increase in adrenal weight in these groups. (4) Adrenal corticosterone content in all the groups but not always adrenal weight, is a fairly accurate reflection of the ACTH levels measured. The results suggest that: (1) Pituitary ACTH content is not a sensitive measure of dynamic changes in synthesis and secretion in rat fetuses. (2) Changes in basal plasma ACTH in response to fetal encephalectomy show the presence of both an autonomous corticotropic function and a cephalic regulation of the corticotropic function from day 16 of fetal life and beyond. Pituitary autonomy seems higher in earlier than in later stages of gestation. (3) There is feedback of corticosterone into the pituitary of fetal rats; a marked increase in ACTH release is caused by the removal of the maternal corticosteroids.