Experiments were performed in female Wistar rats on the mode of action of oestrogen in affecting gonadotrophin secretion during infancy. Using an improved implantation method, former findings on a hypophysial site of oestrogen action in the Hohlweg effect were confirmed. The sensitivity to the ovulation-inducing effect of oestradiol benzoate (OB) increased as the rats approached the age of natural puberty. The first spontaneous ovulation could be suppressed by intrahypophysial, but not by intrahypothalamic, progesterone implants.
A single s.c. injection or intracranial administration of OB at 25 or 26 days of age, although leading to premature vaginal opening (VO) and, in some of the animals, to one ovulation, did not induce true precocious puberty. To accelerate the onset of puberty, 0·05 μg OB/100 g body wt had to be injected daily from 5 days of age to VO, or from day 5 to day 10 and, additionally, from day 26 to VO. After long-term oestrogen treatment, the gonadotrophin-inhibiting effect of OB implanted into the middle hypothalamus from 26 to 34 days of age was significantly reduced in comparison with untreated control rats. A final experiment demonstrated that the first ovarian cycle was not prolonged after neonatal ovariectomy and implantation of ovaries at 24, 28 or 32 days of age. The results indicate that similar neurohormonal mechanisms are operational at the first pubertal and at later cyclic ovulations. They also indicate that the maturation of the gonadotrophin-controlling mechanisms continues during infancy in the absence of ovarian steroids. It can be accelerated in Wistar rats by long-term, but not by short-term prepubertal oestrogen treatment.
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