Post-hypophysectomy ovarian senescence and its relation to the spontaneous structural changes in the ovary of intact aged rats.

Hypophysectomy performed in 25- to 26-day-old Wistar rats leads within 1 years to the formation of ovarian testis-like tubes and epithelial cellular cords which are typical structures in the senile ovaries of normal 24-month-old rats. Testis-like tubes represent an unusual late stage of follicular degeneration; the origin of the cords is more complex; the revival of cell differentiation from stroma and/or rete ovarii in the absence of the pituitary is hypothesized. At 16 months of age, cords proliferate and are responsible for ovarian weight increase to almost twice the minimal weight seen 4 months after the operation. Variability in cord proliferation is considerable from one rat to another, but also between the two ovaries of the same animal. Thus, an intrinsic age-related ovarian factor is implicated in cord proliferation. From this study, it is inferred that during intact rat senescence, intrinsic ovarian aging is responsible for the proliferation of cords, whereas their induction depends on a hypothalamic-hypophyseal imbalance occurring at about 1 year of age.

[Secretion of ovarian estrogen induced by HCG in immature hypophysectomised rats]. / Sécrétion d'destrogène ovarien induite par HCG chez la ratte impubère hypophysectomisée

The daily injection of 50 IU of HCG to immature hypophysectomized Rats does not stimulate follicular growth, even at long term, but causes vaginal estrus of ovarian origin after about 11 to 12 days. The part played by "thecal bodies" induced by HCG in the production of estrogen is discussed.

Light and electron microscopy of the ovarian interstitial tissue in the senile rat: normal aspect and response to HCG of "deficiency cells' and 'epithelial cords'.

The two components of the interstitial tissue in the senile rat's ovary--deficiency cells and epithelial cellular cords--both contain steroidogenic organelles at a very low level of activity, which can be notably raised by HCG. Deficiency cells and epithelial cords are not the expression of primary ovarian aging, but the consequence of senile gonadotropic hypofunctioning. For that same reason, these ovarian structures become permanent and their possible cellular aging can thus be studied. No ultrastructural signs of senescence have as yet been observed.