Testicular Prolactin Receptors Research Articles

Hormonal Regulation of Testicular Prolactin Receptors and Testosterone Synthesis in Golden Hamsters1

A study was conducted with hypophysectomized hamsters to determine effects of administration of prolactin (PRL), luteinizing hormone (LH), and follicle-stimulating hormone (FSH)-alone or in combination-on testicular PRL receptors and in vitro testosterone production. Hormonal injections commenced the second day after hypophysectomy, and hamsters were killed on Day 5, approximately 13 h after the last hormonal injection. PRL receptor numbers were reduced by hypophysectomy, and PRL administration alone lessened the extent of this decrease. By themselves, neither LH nor FSH affected PRL receptors, but a combination of PRL + FSH + LH produced the greatest effect on these receptors. Receptor affinity was only modestly affected by any treatments. In vitro testosterone synthesis was measured after addition of 0, 2, 10, and 50 mIU of human chorionic gonadotropin (hCG) to incubations of testicular tissue. Neither PRL nor FSH by themselves in vivo affected basal or hCG-stimulated testosterone production. However, PRL + FSH increased (p less than 0.05) the magnitude of the in vitro testosterone response to hCG, as well as the sensitivity of that response (slope of the dose-response curve). LH alone increased both basal and hCG-stimulated testosterone production. PRL + LH provided no additional increase in the magnitude of the testosterone response, but increased (p less than 0.05) the sensitivity. PRL + FSH + LH in vivo provided for the greatest sensitivity of the testosterone response to hCG.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of long-term treatment with melatonin or melatonin plus ectopic pituitary transplants on testicular LH/hCG and prolactin receptors in juvenile Syrian hamsters (Mesocricetus auratus).

Juvenile hamsters were injected daily with melatonin and some were also given transplants of 2 pituitaries under the kidney capsule. Weights of the testes and the accessory reproductive glands were reduced after 8 and after 12 weeks of melatonin treatment, but remained unaltered in animals treated with ectopic pituitary transplants. Levels of testicular LH/hCG receptors were significantly reduced by daily melatonin injections for 8 and 12 weeks. The presence of pituitary transplants in melatonin-injected hamsters prevented these reductions, and increased LH/hCG receptors above control levels. These changes in testicular LH/hCG receptors were closely related to alterations in serum prolactin concentration induced by melatonin and pituitary transplants. After 8, but not after 12 weeks of treatment, testicular prolactin receptor levels were reduced by melatonin and maintained by the presence of pituitary transplants. We conclude that: juvenile male hamsters become sensitive to the effects of daily melatonin injections when they reach maturity; daily melatonin injections can reduce the levels of testicular LH/hCG and prolactin receptors; and the effects of melatonin on LH/hCG and prolactin receptors are probably due to suppression of endogenous prolactin release.

Prolactin (PRL), follicle-stimulating hormone, and luteinizing hormone are regulators of testicular PRL receptors in golden hamsters.

The ability of PRL, FSH, and LH to regulate testicular PRL receptors in golden hamsters was evaluated using a variety of experimental protocols. Exposure to a photoperiod of 5 h of light and 19 h of darkness (5L:19D) for 11 weeks precipitated a 94% reduction in content (femtomoles per testes) of testicular PRL receptors and, concomitantly, a decrease (P less than 0.05) in plasma PRL, but not LH or FSH. One pituitary gland under the kidney capsule in 5L:19D-housed hamsters increased (P less than 0.05) both the concentration (femtomoles per mg protein) and content of PRL receptors, as well as those of plasma PRL and FSH. Similar treatment in 14L:10D-housed hamsters produced comparable changes in plasma PRL and FSH without affecting PRL receptors. Injections of L-dopa for 7 days into hamsters housed in 5L:19D for 11 weeks significantly elevated serum FSH concentrations, had no measurable effect on serum PRL and LH, and induced a greater than 2-fold increase in PRL receptor levels. In a separate study, hamsters housed in 5L:19D for 12 weeks were injected for 3 days with 250 microgram ovine (o) PRL, 25 microgram oLH, or 5 microgram oFSH, and results were compared with vehicle-injected, 5L:19D- and 14L:10D-housed controls. Injections of oPRL and oLH increased (P less than 0.05) PRL receptor concentration and content, with PRL being more efficacious. No anti-oPRL antibodies were produced by oPRL injections. In this study, injections of oFSH were without effect on PRL receptors. To ascertain the effects of each hormone in the absence of other trophic influences, experiments were conducted in hypophysectomized hamsters injected daily for 3 days (2-4 days posthypophysectomy) with one of the following: 5 or 25 microgram oLH; 10, 50, or 250 microgram oPRL; or 1 or 5 microgram oFSH. Hypophysectomy reduced the concentration and content of PRL receptors by 85%, and treatment with 50 or 250 microgram oPRL increased (P less than 0.05) these low levels almost 3-fold. Again, no anti-oPRL antibodies were induced. Injection of 5 microgram oLH or 25 microgram oFSH also induced increases (P less than 0.05) in PRL receptors. Hypophysectomy reduced basal and hCG-stimulated in vitro testicular testosterone production (nanograms per testes/4 h) to levels less than 20% of control values. None of the hormonal treatments affected (P less than 0.05) basal testosterone production in vitro.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of different numbers of ectopic pituitary transplants on regulation of testicular LH/hCG and prolactin receptors in the hamster (Mesocricetus auratus).

Adult male hamsters were given transplants of 1/2, 1, 2, 3 or 4 pituitaries under the kidney capsule and were killed 4 weeks later. Pituitary transplants produced a significant, dose-related increase in plasma prolactin levels, no changes in plasma LH and an increase in plasma FSH. Concentration of LH/hCG receptors in the testes was significantly increased in animals with 2 or 3 transplants and concentration of testicular prolactin receptors was significantly increased in those given 2 transplants. The apparent stimulatory effects of 1/2, 1 or 4 transplants on testicular LH/hCG and prolactin binding were not statistically significant. Some of the animals were injected with 0.3 i.u. hCG/g body weight 24 h before being killed. This produced a significant reduction in the levels of prolactin receptors and an apparent reduction in the levels of LH/hCG receptors in the testes. Elevation of plasma testosterone concentrations in response to hCG was significantly greater in animals given 3 or 4 pituitary transplants than in the remaining groups. These results provide further evidence that prolactin increases the number of LH/hCG and prolactin receptors in the hamster testis and suggest that changing the number of ectopic pituitary transplants may result in biphasic effects on the testis, with 2 or 3 transplants being maximally stimulatory.

Testicular Prolactin Receptors and Serum Growth Hormone in Golden Hamsters: Effects of Photoperiod and Time of Day 1

Investigations were conducted to determine effects of exposure to short photoperiod--with its accompanying reductions in serum prolactin (Prl) concentrations--for various durations on testicular Prl receptors. An additional study investigated the possibility of nyctohemeral fluctuations in testicular Prl receptors and serum growth hormone (GH) concentrations and their alteration by photoperiod. After 10 and 28 days of exposure to a short photoperiod consisting of 5 h of light and 19 h darkness (5L:19D) (and prior to changes in testicular weight), there were progressive and significant reductions in the concentration of testicular Prl receptors (fmol/mg protein) when compared with long-photoperiod controls (14L:10D). After 12 weeks of 5L:19D, when testicular weights were dramatically decreased, Prl receptor concentration was reduced to 39% of long-photoperiod controls in one study, without alteration of affinity of Prl receptors for their labeled ligand. When measured at 6-h intervals in hamsters on 14L:10D, and on 5L:19D for 12 weeks, there were no significant changes in concentration or total content (fmol/testes) of testicular Prl receptors throughout the day. Although serum GH concentrations fluctuated markedly in hamsters on both photoperiods, no definitive nyctohemeral patterns were detected. These data provide indirect evidence for the ability of Prl to regulate its own testicular receptors, and demonstrate that diurnal fluctuations in testicular sensitivity to injected Prl are not a consequence of changes in Prl receptors. The data also suggest the absence of effects of photoperiod on serum GH concentrations in male golden hamsters.

Effects of an LHRH agonist and gonadotropins on testicular prolactin receptors

Effects of administration of the LHRH agonist D-Leu 6-LHRH ethylamide (LHRH-A), gonadotropin (PMS), and their interaction on testicular prolactin (PRL) receptor levels were investigated in rats. LHRH-A (2 μg/100 g body wt.) or saline was injected SC daily, and PMS (5 IU) injected every other day. In intact rats, the testicular PRL receptor levels were about 400 fmoles/testis after either 1 or 7 daily injections of saline. Administration of LHRH-A decreased PRL receptors to 12% of that of saline-injected control rats at day 1, and to 20% at day 2, and PRL receptor levels were partially restored to 55% at day 7. In hypophysectomized rats given daily injections of saline for 7 days PRL receptor levels were only 20% of those in saline-injected intact rats. Injections of LHRH-A in hypophysectomized animals did not further decrease PRL receptor numbers at this time. Administration of PMS to hypophysectomized rats for 7 days partially reversed the reduction of PRL receptors that occurred after hypophysectomy, to 46% of those in intact controls. Injections of LHRH-A into hypophysectomized, PMS-treated animals did not significantly alter PRL receptors on day 1 (117% of that of saline-injected, hypophysectomized, PMS-treated rats at day 1) or day 2 (96% of same-day controls), but decreased PRL receptors on day 7 to 102 fmoles/testis (55% of same-day controls). This latter concentration is nearly the same as that in saline-injected, 7-day hypophysectomized rats not treated with PMS. These findings suggest that: (1) the effects of LHRH-A on testicular PRL receptors differ depending on the presence or absence of gonadotropin, (2) gonadotropin, primarily FSH, maintains some population of testicular PRL receptors, and these gonadotropin-dependent PRL receptors are suppressed by direct action of LHRH-A upon the testes, and (3) there is a population of PRL receptors which is not affected by LHRH-A or gonadotropin.

Regulation of adrenal and testicular prolactin receptors by adrenocorticotropin and luteinizing hormone.

Receptors for PRL in the adrenal, ovary, and testis undergo marked and rapid depletion after trophic stimulation by ACTH and LH, respectively. The mechanism of such heterologous regulation of PRL receptors in the testis and adrenal cortex was further analyzed in hormone-treated male rats. Hormone-stimulated turnover of PRL receptors was not prevented by treatment with cycloheximide (75 and 300 μg), which caused an 80% fall in testicular and adrenal sites within 1 h, followed by a return to normal in 24 h. When steroid secretion was inhibited by treatment with 4-aminopyrazolopyrimidine for 4 days, with a 90% decrease in serum cholesterol, ACTH and LH retained the ability to reduce PRL receptors by 60–70% 12 and 24 h after injection. Similarly, during blockade of steroidogenesis by aminoglutethimide, treatment with 10 U ACTH or 100 μg ovine LH still reduced PRL receptors by about 70%. When adrenal and testicular steroidogeneses were stimulated by the administration of 8-bromo cAMP, serum corticosterone and ...

Stimulatory effect of luteinizing hormone and human chorionic gonadotropin on testicular prolactin receptor levels.

A possible effect of LII or hCG on testicular prolactin receptor levels was investigated in hypophysectomized adult rats. Hypophyseetomy leads to a progressive decrease of testicular prolactin receptor content to ‘\�25% of that of controls 12 days after surgery. In animals injected3 times a day for 10 days with highly purifiedpreparations of ovine LII or hCG, prolactin receptor levelsincreasedfrom 21 4 to 41 ± 4 and 71 7 fmol/testis, respectively (P<0.01 for both). The increase in the number of testicular prolactin receptor levels observed after treatment with hCG in hypophysectomized rats could not be duplicated by injection of estradiol-173 (0.5 pg), testosterone (200 pg) or 5u-dihydrotestosterone (200 pg) given twice a day for 5 days. Moreover, these steroids do not interfere with the stimulation of prolactin binding induced by hCG. Since treatment with prolactin is well known to stimulate testicular LII binding and steroidogenesis, the present data provide further evidence for a close interaction between prolactin and LII in the control of the testicular levels of receptors for these two hormones and their subsequent role in the control of testicular functions.

Lactogenic receptor regulation in hormone-stimulated steroidogenic cells

Receptor sites for lactogenic hormones such as prolactin (PRL), human growth hormone (HGH), and placental lactogens, are widely distributed in mammalian tissues, including mammary glands, steroid-secreting cells of the adrenal, testis, and ovary, and target cells of steroid hormone action such as liver, prostrate, and kidney. Although the biological functions of lactogen binding sites remain uncertain, a relationship between prolactin and lipoprotein metabolism is implied by the occurrence of prolactin receptors in steroidogenic cells of the gonads and adrenal, and by the ability of prolactin to increase esterified cholesterol in the testis. Recently, loss of testicular prolactin receptors has been observed following elevation of circulating luteinising hormone (LH) concentrations by the gonadotropin releasing hormone (GnRH) and its agonist analogues. The hormone dependence of lactogen receptor sites in steroid-secreting cells was further analysed in rat testis, ovary, and adrenal glands after treatment with the respective trophic hormones, gonadotropin and ACTH. In each of these tissues, rapid and transient loss of lactogen receptors was observed after trophic hormone stimulation. These findings indicate that increased turnover of lactogen receptors is an important component of the target-cell response, and suggest that prolactin receptors might be involved in the transport of lipoprotein precursors for steroid biosynthesis.

Effect of prolactin and growth hormone on prolactin and LH receptors in the dwarf mouse

Dwarf mice (DW/J;dw/dw) which exhibit a deficiency of prolactin and GH secretion were treated for 8 days with ovine prolactin and/or human GH (10 or 20 mug/day) and the effect on hepatic and testicular prolactin receptors was investigated. In both sexes there was a significant increase in body weight after all hormone treatments, but an increment in testicular weight was observed only after prolactin administration. Prolactin treatment increased the specific binding % of prolactin in liver membranes in females but not males, and in testicular homogenates (together with an increase in LH receptors). The results suggest that lack of prolactin but not of GH retards sexual development in these mice. Treatment with prolactin partly counteracts this deficiency, and the effect may be mediated by the induction of hepatic and testicular prolactin and LH receptors.