TL;DR: It is suggested that Adrenalectomy or sham adrenalectomy retards the postcastration rise in gonadotropins by preventing the immediate expansion of the granulated cell population and causing an apparent loss in the numbers of certain types of Gonadotropes.
Abstract: Castration produces hypertrophy of gonadotropes, stimulates a shift in storage patterns to cells that store LH and FSH together, and results in a significant rise in serum LH and FSH within 12 h. Adrenalectomy retards and attenuates this postcastration rise for 24 h (1,2). In this study, we examined the effect of adrenalectomy on castration cell morphological development. The increased percentages of LH and FSH cells that are seen normally 24 h after castration were not seen if adrenalectomy or sham adrenalectomy was performed simultaneously. In fact, the percentages of LH cells were below control values. The expansion in the average area of LH and FSH cells was also retarded after simultaneous castration and adrenalec-tomy or sham adrenalectomy. The corticotrope population responded as expected to adrenalectomy and the surgical stress of castration, with an increase in the percentage and area of stained cells as well as partial degranulation. The serial sections showed no ACTH staining in gonadotropes af...
TL;DR: Addison in 1917, using male rats, presented a more complete histologieal analysis of the changes occurring in the anterior hypophysis after castration, and described an early increase in the number and size of the basophiles, the larger ones becoming vacuolated in two months afterCastration.
Abstract: Although changes following castration were described in the anterior pituitaries of cattle, buffaloes and fowls as early as 1905 (Fichera), the earliest investigation on the effect of castration on the anterior pituitary of the albino rat was that of Zacherl reported by Biedl in 1912. He described an increase in the volume of the organ and a diminution in the number of aeidophiles, but of most interest was his description of a new cell type which he designated as a castration cell. He did not determine the origin of this new cell type. Addison in 1917, using male rats, presented a more complete histologieal analysis of the changes occurring in the anterior hypophysis after castration. He described an early increase in the number and size of the basophiles, the larger ones becoming vacuolated in two months after castration. With the increase in the size and number of these vacuoles, the cytoplasm and nuclei were pushed to the side, producing the typical castration cell or “signet-ring” cell. Colloid fillin...
TL;DR: Estradiol contained within the lumen of 30 gauge hypodermic tubing was implanted into the arcuate nucleus, mammillary bodies, or anterior lobe of the pituitary, either at the time of spaying or 11 days or 60 days after castration.
Abstract: Estradiol contained within the lumen of 30 gauge hypodermic tubing was implanted into the arcuate nucleus, mammillary bodies, or anterior lobe of the pituitary, either at the time of spaying or 11 days or 60 days after castration. The normal pituitary weightand cytological characteristics of the gonadotrophs were maintained only when estradiolwas implanted in the arcuate nucleus after spaying. Blank tubing implants in all the previously mentioned locations or estradiol implants in the mammillary bodies or anteriorpituitary were completely ineffective in inhibiting the typical sequence of castration cell formation which occurs in the pituitary of the spayed rat.
TL;DR: Estrogen can inhibit gonadotrophin secretion in rats which lack the hypothetic “steroid receptors” said to exist in the anterior hypothalamus in rats with and without that part of the hypothalamus which Flerkd reported to be essential for the inhibitory action of estrogen on gonadotropic secretion.
Abstract: Three estrogenic regimens (0.1, 1.0 and 5.0 μg of estradiol benzoate/day for 30 days) were used to inhibit pituitary castration cell development. Each appeared equally effective in rats with and without that part of the hypothalamus which Flerkd reported to be essential for the inhibitory action of estrogen on gonadotrophin secretion. This demonstrates that estrogen can inhibit gonadotrophin secretion (at least gonadotrophin synthesis) in rats which lack the hypothetic “steroid receptors” said to exist in the anterior hypothalamus. The interpretation of these findings is discussed.
TL;DR: The results offer a morphological basis to the adoption of a biphasic effect of alcohol on gonadotropic secretion in rats which received a 15% solution of ethyl alcohol for 6 months.
Abstract: Histological and ultrastructural changes of hypophyseal gonadotropic cells of rats which received a 15% solution of ethyl alcohol for 6 months were studied. Light microscopy revealed hyperplasia and h