Prolactin

About: Prolactin is a research topic. Over the lifetime, 22356 publications have been published within this topic receiving 609537 citations. The topic is also known as: lactotropin, & PRL,.

Prolactin release during nursing and breast stimulation in postpartum and nonpostpartum subjects.

Abstract: The effect of suckling and breast stimulation on plasma prolactin measured by homologous radioimmunoassay has been studied in nursing women, in normal, nonlactating women and men, in chlorpromazine treated women, in pregnant women, and in women with galactorrhea. Nursing women had increased plasma prolactin before nursing during the first 6 weeks postpartum; mean prolactin rose rapidly throughout the period of suckling and reached a peak 8.5 times the baseline value just after the termination of nursing. Women studied between 7 and 28 weeks postpartum had normal prolactin levels before nursing; with suckling they had smaller but significant elevations, averaging 6.0 times the baseline value at the end of nursing. When nursing women were allowed to play with but not nurse their infants, prolactin did not rise in spite of the occurrence of milk let-down. Substitution of a breast pump for the infant at a regular period of nursing caused prolactin elevations similar in timing and in magnitude to thos...

Endocrinological and catecholaminergic alterations during sleep deprivation and recovery in male rats.

Abstract: Since previous data of our group showed increased concentrations in HPA axis hormones in sleep deprived rats, we hypothesized that this augmentation could produce effects in other hormonal systems, particularly in the sexual system. Considering that little is known about how the hormonal system changes during the recovery period after sleep deprivation (SD), our objective was to examine from what point SD alters sexual and stress-related hormones along with plasma catecholamine concentrations during 4 days. We also sought to verify the time course of their recovery after an equivalent period of recovery sleep. Rats were deprived of sleep by the platform technique for 1-4 days and were allowed to recover for the same period. Plasma catecholamines [dopamine (DA) and noradrenaline (NOR)], testosterone, estrone, progesterone, prolactin, corticosterone and adrenocorticotropic hormone (ACTH) concentrations were measured. Comparisons between groups showed that the SD procedure used in the present study produced marked alterations in almost all studied hormones from 24 h of SD, except for estrone and prolactin (which required 96 h of SD to become altered). Testosterone and estrone decreased, whereas progesterone, prolactin, corticosterone, ACTH, DA and NOR increased. During recovery period, progesterone, prolactin and corticosterone concentrations returned to control levels, whereas testosterone, estrone, NOR and DA did not. In addition, after 48 h of recovery ACTH and NOR decreased below control concentrations, remaining low until 96 h of sleep recovery. Thus, SD showed long lasting, differential effects upon these neurochemicals suggesting that each has its own pattern of responses to SD as well as variable periods of recovery.

Prolactin, growth hormone, and luteinizing hormone in the maintenance of testicular luteinizing hormone receptors.

Abstract: To elucidate further pituitary influence on testicular function, we studied the effect of PRL, GH, and LH alone or in various combinations on the maintenance of testicular LH receptor concentration and testosterone synthesis in response to LH (testicular responsiveness) in hypophysectomized adult rats. Hypophysectomy reduced LH receptor concentration by 80% and testicular responsiveness to LH by 70% 7 days after surgery. Treatment with PRL (75 or 150 μg/day) or with GH (75 or 150 μg/day) initiated within 6 h after surgery and continued twice daily for 6 days partially prevented the loss of LH receptors. The effect of PRL (150 μg/day) plus GH (150 μg/day) on LH receptor concentration was additive. The combination of LH (5 μg/day), PRL, and GH prevented any loss of LH receptors after hypophysectomy. A positive effect of LH on its receptor occurred in the presence of PRL. Treatment of hypophysectomized rats with 5 /μg LH plus 150 /μg PRL enhanced the effect observed with PRL alone (1.31 pmol/testis vs. 1.68 ...

The Pituitary Gland in Pregnancy: A Clinicopathologic and Immunohistochemical Study of 69 Cases

Abstract: A histologic and immunocytochemical study of 69 autopsy-obtained pituitaries from women who died during pregnancy, after abortion, or in the postpartum period revealed an accumulation of large chromophobic to slightly acidophilic and periodic acid-Schiff-negative pregnancy cells that were immunoreactive for prolactin but not for other pituitary hormones. This increase in the number of prolactin cells was confirmed by cell counts. Thus, pregnancy cells are capable of prolactin production. The finding of mitotic figures in such cells supports the view that they arise by multiplication from preexisting prolactin cells. With use of "mirror section" techniques, no mammosomatotrophs (cells immunoreactive for growth hormone and prolactin) were identified. Hyperplasia of prolactin cells was evident at 1 month of pregnancy and gradually disappeared within several months after delivery or abortion; the process of involution seemed to be retarded in the one lactating patient investigated. In some pituitaries, the accumulation of prolactin cells was so extensive that the hyperplastic foci resembled microadenomas. Another striking change in the pituitaries of pregnant women was appreciable reduction of immunostaining of gonadotropic cells, a process that was reversible as soon as 1 month after delivery. Among the 69 pituitaries studied, 8 noninvasive microadenomas (12%) were encountered (7 contained prolactin only and 1 was plurihormonal). Prolactin-producing adenomas were no more numerous or larger than were similar tumors encountered in nonpregnant women or normal men; thus, pregnancy neither initiates formation of pituitary adenomas nor accelerates their growth. In the pituitaries that harbored prolactin-producing adenomas, massive pregnancy cell hyperplasia was evident outside the tumor; thus, prolactin production by adenoma cells did not seem to suppress the proliferation of prolactin-containing pregnancy cells.

Activation of JAK2 tyrosine kinase by prolactin receptors in Nb2 cells and mouse mammary gland explants

Abstract: One of the earliest cellular responses to prolactin (PRL) binding in Nb2 cells, a rat pre-T lymphoma cell line, is an increase in tyrosine phosphorylation of cellular proteins. In this work, immunologic techniques have been used to demonstrate that in Nb2 cells and in mouse mammary gland explants, JAK2, a non-receptor tyrosine kinase, is activated following stimulation with PRL. PRL stimulated tyrosine phosphorylation of JAK2 at times as early as 30 sec and concentrations of PRL as low as 0.5 ng/ml (2.5 pM) in Nb2 cells and 100 ng/ml (5 nM) in mammary gland explants. When JAK2 was immunoprecipitated from solubilized Nb2 cells or mammary gland explants and incubated with [gamma-32P]ATP, 32P was incorporated into a protein migrating with an apparent molecular weight appropriate for JAK2 only when cells had been incubated with PRL, indicating that JAK2 tyrosine kinase activity is exquisitely sensitive to PRL. In Nb2 cells, JAK2 was found to associate with PRL receptor irrespective of whether or not the cells had been incubated with PRL. These results provide strong evidence that JAK2 is constitutively associated with the PRL receptor and that it is activated and tyrosine phosphorylated upon PRL binding to the PRL receptor. These results are consistent with JAK2 serving as an early, perhaps initial, signaling molecule for PRL.