We analysed cell types in the pars distalis of normal young adult male and female rats with respect to their percentages and the relative volumes they occupy. In male rats the percentages of the cell types were: prolactin 49.80, GH 22.67, LH 5.04, FSH 4.22, ACTH 2.93 and TSH 2.09. The volume densities were: prolactin 20.48, GH 20.95, LH 7.34, FSH 6.73, ACTH 3.75 and TSH 3.19. In female rats the percentages of the cell types were: prolactin 52.40, GH 20.30, LH 5.89, FSH 4.06, ACTH 2.53, TSH 2.40 and the volume densities were: prolactin 28.09, GH 20.86, LH 8.11, FSH 5.46, ACTH 3.49 and TSH 2.91. The percentages of pars distalis cells which did not stain with the antisera to the six classical hormones were 17.47 in male and 16.48 in female rats. The results suggest that (1) in both sexes the number (N) of prolactin cells greater than N of GH cells greater than N of gonadotrophs greater than N of TSH or ACTH cells, (2) the percentage of each cell type was similar in both sexes, (3) the volume density (Vv) of prolactin cells was greater than the Vv of GH cells in female but not in male rats and in both sexes the Vv of GH cells greater than the Vv of gonadotrophs greater than the Vv of TSH or ACTH cells, (4) in both sexes the volume (V) of prolactin cells less than the V of GH cells less than the V of gonadotrophs, the V of TSH cells or the V of ACTH cells, (5) the V of prolactin cells was greater in female than in male rats and (6) approximately 17% of the cells in the pars distalis of both sexes did not contain 'immunoreactive' prolactin, GH, LH, FSH, TSH or ACTH.
We investigated whether 1) the absolute or the relative numbers of LH and FSH cells change during the rat estrous cycle, 2) the percentages of gonadotrophs that contain LH and/or FSH change during the estrous cycle, and 3) gonadotrophs change in size during the rat estrous cycle. Groups of four female rats were decapitated at one of five different times during the estrous cycle. Four male rats were also decapitated. Serum concentrations of LH and FSH were determined by RIA. Paired horizontal flip-flopped or nonflipped paraffin sections were mounted from the dorsal, middle, and ventral portions of each pituitary gland. In each pair of sections, one was stained with a-rat LH-S4 and the other with a-rat FSH-S7 by the unlabeled antibody peroxidase-antiperoxidase method. All immunoreactive cells were counted. Photographs were taken from randomly chosen corresponding areas, and the cells were individually matched to determine the percentage that contained one or both hormones. Correction factors had to be used because in paired flip-flopped or nonflipped sections stained with the same antibody (a-rat LH-S4), not all of the stained cells found in one section were found in the other section. The absolute numbers of LH and FSH cells did not change throughout the estrous cycle. The ratio of LH cells to FSH cells in the pars distalis of female rats was also constant throughout the estrous cycle. In female rats, 75.2% of LH cells also contained FSH, while 99.4% of FSH cells also contained LH. In the male rats, 88.6% of LH cells also contained FSH, while 98.6% of FSH cells also contained LH. Similar results were obtained in paired flip-flopped sections stained with a-rat LH beta and a-rat FSH beta. Sequential staining of additional individual tissue sections with a-rat LH-S4 and then a-rat FHS-S7 or vice versa revealed the following. Staining of LH-stained tissue for FSH revealed less than 1% new cells, but staining of FSH-stained tissue for LH revealed a 8.7% increase in gonadotrophs in males and a 25.4% increase in females. The gonadotrophs in female rats did not change in size during the estrous cycle and were significantly smaller than the gonadotrophs in male rats. The results suggest that in normal adult rats: 1) virtually all FSH-containing cells contain LH, 2) about 25% of the gonadotrophs in females and about 11% of the gonadotrophs in males contain LH but not FSH, 3) the number of cells containing LH or those containing LH and FSH does not change during the estrous cycle, 4) gonadotrophs in female rats do not change in size during the estrous cycle and are smaller than the gonadotrophs in male rats, and 5) FSH release during the early morning of estrus, when the serum FSH concentration is elevated and the serum LH concentration is low, occurs from cells that contain both LH and FSH.
We investigated the influence of LHRH on the differentiation of gonadotrophs and lactotrophs in fetal pituitary glands transplanted beneath the renal capsules of adult hypophysectomized-orchidectomized hamsters (hosts). Hypophyses were removed from hamster fetuses at a gestational age of 14 days. Some of these were immediately fixed in Bouin's solution, and others were transplanted into the hosts. The hosts were injected sc twice daily with 1 microgram LHRH or vehicle for 16 days. Six hosts in each group were killed by decapitation 16 h after the last injection. Six 14-day-old normal male hamsters (age-matched to correspond to the age of the allografts at the time of the hosts' decapitation) also were decapitated. Sections of hypophyses in situ from fetal hamsters, from 14-day-old controls, and from allografts in each group were stained for LH, FSH, or PRL and with hematoxylin. No PRL-containing cells and very few LH or FSH cells (less than 0.025% of the adenohypophysial cell population) were observed in fetal pituitary glands. In allografts from the vehicle-treated hosts, 21.1% of adenohypophysial cells contained LH, but only 1.8% contained FSH. In allografts from LHRH-treated hosts, 28.0% and 22.9% of the adenohypophysial cells contained LH and FSH, respectively. Adenohypophyses that developed for the same length of time in situ had smaller percentages of adenohypophysial cells containing LH (23.8%) and FSH (15.5%) than the LHRH-treated group. LH-containing cells in allografts in the vehicle-treated hamsters, but not in the LHRH-treated animals, were reduced in size compared to those measured in situ. The number of lactotrophs in all allografted tissue was markedly reduced compared to that of lactotrophs in situ, and injection of LHRH into hamsters with allografts did not alter the percentage of adenohypophysial cells that were lactotrophs. These results suggest that in the hamster LHRH 1) plays an important role in stimulating the formation of immunoreactive FSH in the pituitary gland, 2) can increase the number of gonadotrophs that develop during the neonatal period, and 3) plays a role in controlling the size of gonadotrophs during development. The results also suggest that the development of lactotroph cell number requires close proximity to the hypothalamus and/or exposure to a neonatal environment. We found no evidence to support the view that LHRH, LH, or FSH stimulates immunoreactive lactotroph differentiation.
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