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T. Harigaya, S. Sakai, K. Kohmoto, and Y. Shoda

Regulation of mammary prolactin receptors by steroid hormones was investigated in ovariectomized mid-pregnant mice. Ovariectomy increased the number of mammary prolactin receptors per cell with no effect or a slight decrease in dissociation constant (K d). The simultaneous removal of adrenals prevented this increase in numbers. A single injection of glucocorticoid (corticosterone or cortisol) in ovariectomized–adrenalectomized mice restored the number of prolactin receptors in mammary glands to the same level as that in ovariectomized controls without changing the K d. Aldosterone, deoxycorticosterone and oestradiol did not affect the number of mammary prolactin receptors after ovariectomy–adrenalectomy. Serum concentration of prolactin was not influenced by the hormone manipulation except with injections of oestradiol or cortisol and apparently did not correlate with the number of prolactin receptors. These results indicated that glucocorticoids are required for the increase in the number of mammary prolactin receptors induced by ovariectomy in mid-pregnant mice.

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M. Nonomura, K. Hoshino, T. Harigaya, H. Hashimoto, and O. Yoshida


Hyperprolactinaemia induced by pituitary isografts in male host mice was confirmed by radioimmunoassay, but plasma testosterone levels determined by radioimmunoassay in these mice showed no changes. Immunoenzyme electron microscopic observations revealed large spherical-shaped immunoreactive prolactin granules in pituitary grafts in male hosts, regardless of the sex of the donor mice, indicating the disappearance of sexual dimorphism in prolactin-producing cells in hyperprolactinaemic mice. In hyperprolactinaemic host mice the male accessory sex glands, particularly the seminal vesicle and the ventral prostate, exhibited considerable proliferation and significant increase in weight. These phenomena do not seem to be mediated by the increased action of testosterone. Such biological effects in host mice were much greater when the donor was female rather than male, and were more noticeable in C57BL mice than in C3H mice.

J. Endocr. (1985) 107, 71–76

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K Horiguchi, S Yagi, K Ono, Y Nishiura, M Tanaka, M Ishida, and T Harigaya

Prolactin (PRL) is a single-chain polypeptide hormone that is generally secreted from prolactin cells of the anterior pituitary gland into the blood circulation. However, recent studies indicate that the gene expression of prolactin is ectopic in several tissues across several species. These studies found that lymphocytes also produce PRL, which is involved in the immunoregulatory system. Here, we searched for PRL messenger ribonucleic acid (mRNA), using the reverse transcriptase-polymerase chain reaction (RT-PCR) and Southern blotting in the spleens of mice at various growth stages. We also localized mouse prolactin (mPRL) and its mRNA in the spleens of 30- and 60-day-old mice by immunohistochemistry and in situ hybridization respectively. The mPRL gene was expressed in all spleen samples at 0–60 days postpartum. We localized mPRL mRNA in the sheathed artery, periarterial lymphatic sheath and the marginal zone of the spleen. Moreover, we detected mPRL in essentially the same area as its mRNA. Furthermore, we performed double-fluorescence immunohistochemical staining for mPRL and mouse CD4 that is specifically produced in helper T cells, or for mPRL and mouse CD19 or CD40 specified B cells. We colocalized mPRL immunoreactivity only in some CD4-immunopositive cells. These results clearly suggest that T cells synthesize mPRL in the mouse spleen.