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It is well known that, in rodents, oestrogen stimulates the activity of the prolactin-producing (LTH) cells of the adenohypophysis. Neonatal administration of oestrogen accelerates the initial appearance of this type of cell (Yamashita, 1969) and a markedly higher population of LTH cells occurs in adult female mice than in males (Yamada, Sano & Ito, 1957; Yamashita, 1969). This would indicate that oestrogen is concerned with the differentiation of prolactin-producing cells. It is not clear, however, whether or not this ovarian hormone is indispensable for the differentiation of LTH cells during ontogeny. The present study is concerned with the clarification of this problem.
We intended to deprive SMA strain mice of oestrogen. The ovary, testis and adrenal cortex are accepted as the main sources of endogenous oestrogen, and at first gonadectomy was performed in male animals. Taking into account the fact that, in the mouse, pituitary LTH cells are not present
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To clarify the role of the ovary in the sexual differentiation of prolactin and growth hormone cells, the anterior pituitary glands of mice ovariectomized before or after puberty were studied by a stereological morphometric technique with the electron microscope. A marked sex difference was observed in the relative proportions of these two types of cells in normal adult control animals. In male mice about 52% of anterior pituitary cells were growth hormone cells and about 10% were prolactin cells, while in female mice prolactin cells represented about 39% and growth hormone cells about 37% of the anterior pituitary cell population. Ovariectomy before puberty reduced the proportion of prolactin cells to about 10% and increased growth hormone cells to about 50% of the cell population. The size of prolactin cells and the development of their cell organelles was also reduced. Ovariectomy after puberty had less marked effects. These results suggest that ovariectomy before puberty induced the male phenotype by inhibition of the differentiation of prolactin cells and stimulation of the differentiation of growth hormone cells. The significance of these results in relation to the sexual differentiation of the pituitary gland is discussed.
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To study the effect of the ovary on sexual differentiation of somatotrophs and lactotrophs, the anterior pituitary glands of castrated adult male mice which had received an ovarian transplant during postnatal development were studied using a stereological morphometric technique with an electron microscope. In adult male mice which were castrated neonatally and given ovarian transplants at the age of puberty (NCT-males), the ovaries contained follicles and corpora lutea. The percentages (∼40) and numbers (∼2 × 105) of lactotrophs were similar in normal dioestrous females and NCT-males, but were higher than the percentage (9·3) and number (4·6 × 104) in normal males. Ovarian grafts in adult male mice which were simultaneously castrated and given an ovarian transplant just before puberty (PCT-males) contained numerous follicles of various sizes but no corpora lutea. The percentage (46·8) and number (3·9 × 105) of lactotrophs were greater in these mice than in dioestrous females. The percentage of somatotrophs in NCT-males (34·7) was less than in normal males (52·6), but was similar to that in dioestrous female mice (37·4). The percentage of somatotrophs in PCT-males (27·4) was less than in normal male and dioestrous female mice. These data indicate that lactotrophs and somatotrophs differentiate to the female phenotype when a cyclically functional ovary is present after puberty.
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ABSTRACT
The effect of phorbol ester pretreatment on rat (r) GH release induced by GH-releasing factor (GRF) or 8-bromo-cyclic (c)AMP was investigated using rat pituitary cells cultured in monolayers. Pretreatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) for 3 h significantly suppressed the rGH release induced by GRF, but not that by 8-bromo-cAMP 20 h later; this suppressive effect of TPA was concentration-dependent from 8 to 160 nmol/l, and complete suppression was observed after pretreatment with 80–160 nmol TPA/l. Production of cAMP by pituitary cells stimulated with GRF was similarly attenuated in TPA-pretreated cells. The rGH responsiveness to GRF of these cells was fully recovered on prolonged culture (40 h), suggesting that the inhibitory effect of TPA is reversible.
In contrast, pretreatment with GRF (5 nmol/l) resulted in suppression of the rGH response to subsequent exposure to GRF (5 nmol/l) or 8-bromo-cAMP (10 mmol/l), but not to TPA. These observations suggest that pretreatment with TPA modifies the rGH response to GRF at steps before the formation of cAMP.
J. Endocr. (1988) 118, 423–428
