Selective release of follicle-stimulating hormone by 5 alpha-dihydroprogesterone in immature ovariectomized estrogen-primed rats

The effect of 5 alpha-dihydroprogesterone (5 alpha-DHP) on gonadotropin release was examined in the immature acutely ovariectomized (OVX) rat primed with a low dose of estradiol (E2). Treatment with various doses of 5 alpha-DHP given in combination with E2 increased levels of follicle-stimulating hormone (FSH) but had no effect on serum luteinizing hormone (LH). A single injection of a maximally stimulating dose of 5 alpha-DHP (0.4 mg/kg) stimulated increases in serum FSH at 1200 h and, 6 h later, at 1800 h. Pituitary LH and FSH content was dramatically enhanced by 1600 h and levels remained elevated at 1800 h. The administration of pentobarbital at 1200 h, versus 1400 h or 1600 h, prevented the increase in basal serum FSH levels at 1800 h, implying that the release of hypothalamic LH releasing hormone (LHRH) is modulated by 5 alpha-DHP. In addition, changes in pituitary sensitivity to LHRH as a result of 5 alpha-DHP were measured and a significant increase in the magnitude of FSH release was observed at 1200 h and 1800 h. Although the LH response to LHRH in 5 alpha-DHP-treated rats was not different from controls, the duration of LH release was lengthened. These results suggest that 5 alpha-DHP may stimulate FSH release by a direct action at the pituitary level. Together, these observations support the theory that 5 alpha-DHP mediates the facilitative effect of progesterone on FSH secretion and further suggests an action of 5 alpha-DHP in this phenomenon at both pituitary and hypothalamic sites.     

Alterations in the proestrous pattern of median eminence LHRH, serum LH, FSH, estradiol and progesterone concentrations in middle-aged rats

The purpose of the following study was to assess the changes in the proestrous hormone profile in middle-aged cycling rats to better understand the inter-relationship and possible interaction of these hormones during the transition to estrous acyclicity. Median eminence LHRH concentrations and serum LH, FSH, estradiol and progesterone concentrations were measured in young (3-4 months old) and middle-aged (8-10 months old) proestrous rats at 0900, 1200, 1500 and 1800h. The data demonstrate that (1) baseline hormone concentrations prior to the surge at 0900h are the same in middle-aged and young rats; (2) the proestrous gonadotropin surge is temporally delayed in middle-aged rats; (3) this delay is preceded by lower median eminence LHRH concentrations and serum estradiol concentrations at 1200h; (4) serum progesterone concentrations are lower in middle-aged rats during the preovulatory gonadotropin surge (at 1500 and 1800h) probably as a consequence of the delayed LH surge.     

Selective release of follicle-stimulating hormone and luteinizing hormone by 5 alpha-dihydroprogesterone and 3 alpha, 5 alpha-tetrahydroprogesterone in pregnant mare's serum gonadotropin-primed immature rats exposed to constant light

The effects of 5 alpha-dihydroprogesterone (5 alpha-DHP) and 3 alpha, 5 alpha-tetrahydroprogesterone (3 alpha, 5 alpha-THP) on follicle-stimulating hormone (FSH) and luteinizing hormone (LH) release were examined in the pregnant mare's serum gonadotropin (PMSG)-primed immature female rat (8 IU PMSG at 28 days of age) maintained in constant light. Control rats kept in 14L:10D conditions exhibited proestrous-like surges of LH and FSH release with peak levels attained at 1800 h on the second day after PMSG treatment. In rats exposed to constant light, the PMSG-induced surges of LH and FSH were not only delayed until 1000 h on the third day after PMSG, resulting in a delay in ovulation, but were also significantly attenuated when compared to the gonadotropin surges that occurred on Day 2 in rats kept under normal light-dark conditions. The administration of 5 alpha-DHP significantly enhanced the release of FSH at 1000 h on Day 3 when compared to constant light-exposed controls, but had no effect on LH. Treatment with 3 alpha, 5 alpha-THP selectively potentiated the release of LH at 1000 h on Day 3 and had an attenuating effect on FSH release on Days 2 and 3. These observations confirm earlier findings in the immature ovariectomized estrogen-primed rat and suggest that 5 alpha-DHP and 3 alpha, 5 alpha-THP may have significant roles in the regulation of FSH and LH secretion.     

A change in basal FSH release accompanies the onset of the second or selective phase of increased serum FSH in the cyclic rat

Experiments were undertaken to investigate if changes occur at the level of the anterior pituitary gland to result in selective follicle-stimulating hormone (FSH) release during late proestrus in the cyclic rat. At 1200 h proestrus, prior to the preovulatory luteinizing hormone (LH) surge in serum and the accompanying first phase of FSH release, serum LH and FSH concentrations were low. At 2400 h proestrus, after the LH surge and shortly after the onset of the second or selective phase of FSH release, serum LH was low, serum FSH was elevated about 4-fold, pituitary LH concentration was decreased about one-half and pituitary FSH concentration was not significantly decreased. During a two hour $\text{in}$$\text{vitro}$ incubation, pituitaries collected at 2400 h released nearly two-thirds less LH and 2.5 times more FSH than did pituitaries collected at 1200 h. Addition of luteinizing hormone releasing hormone (LHRH) to the incubations caused increased pituitary LH and FSH release. However, the LH and FSH increments due to LHRH in the 2400 h pituitaries were not different from those in the 1200 h pituitaries. The results indicate that a change occurs in the rat anterior pituitary gland during the period of the LH surge and first phase of FSH release which results in a selective increase in the basal FSH secretory rate. It is suggested that this change is primarily responsible for the selective increase in serum FSH which occurs during the second phase of FSH release.     

Comparison of estrogen priming effects with body weight restoration effects on the gonadotropin pattern of patients with anorexia nervosa

Plasma estradiol (E2), serum LH and FSH, and the gonadotropin response to two consecutive LHRH administrations (10 and 100 micrograms with an interval of 2 h) were determined in 19 patients with anorexia nervosa (AN) at the emaciation phase, before and after estradiol benzoate (E2B) injections (3 micrograms/kg/day for 7 days). The same investigations were repeated after weight restoration in 9 AN patients who remained amenorrheic. Both at the emaciation phase and after weight restoration, E2B enhanced the second LH response to LHRH and decreased serum FSH, suggesting that the functional capacities of the pituitary gonadotrophs are normal in AN. Unlike E2B injections, weight restoration increased all the hormone values, suggesting that the weight restoration effects on the abnormal gonadotropin secretory pattern of AN depend on another mechanism than the E2 lowering. That mechanism is probably a disorder of the hypothalamic LHRH secretion, the consequences of which could be reinforced by the low E2 levels.     

Ovulation inhibition in the pregnant mare's serum gonadotropin-treated immature rat: a bioassay for luteinizing hormone-releasing hormone antagonists

A convenient method for evaluating the biological activity of luteinizing hormone-releasing hormone (LHRH) antagonists was devised. Pregnant mare's serum gonadotropin (PMSG) treatment of immature rats is known to stimulate follicular growth and estrogen production, that in turn stimulates the release of LHRH which triggers an ovulatory discharge of luteinizing hormone (LH) from the pituitary. The present bioassay of the antagonists is based on the inhibition of ovulation in the PMSG-treated rats. Twenty-eight-day-old Sprague Dawley rats maintained under a light period of 12 h/day (lights on at 0630 h) were given 10 IU of PMSG s.c. at 0930 h. On Day 30 of age the antagonist was given s.c. at 1430 h. The rats were killed on the following morning and the oviducts examined for the presence of ova. In addition, the antagonists were compared in their ability to inhibit serum testosterone levels in adult male rats. In the PMSG-treated rats the order of ovulation-inhibiting potency of the following antagonists was: [Ac-D-NAL(2)1,4FD-Phe2,D-Trp3,D-Arg6]-LHRH (LHRH-1) greater than [Ac-delta 3 Pro1,4FD-Phe2,D-NAL(2)3.6]-LHRH (LHRH-2) greater than [Ac-delta 3 Pro1,4FD-Phe2,D-Trp3,6]-LHRH (LHRH-3). The order of potency was confirmed by their antitesticular effects in adult male rats.     

Hypersecretion of follicle-stimulating hormone (FSH) on estrous afternoon in rats treated with RU486 in proestrus

Summary 1. Intact or ovariectomized (OVX) cyclic rats injected or not with RU486 (4 mg/0.2 ml oil) from proestrus onwards were bled at 0800 and 1800h on proestrus, estrus and metestrus. Additional RU486-treated rats were injected with: LHRH antagonist (LHRHa), estradiol benzoate (EB) or bovine follicular fluid (bFF) and sacrified at 1800 h in estrous afternoon. LH and FSH serum levels were determined by RIA.2. RU486-treated intact or OVX rats had decreased preovulatory surges of LH and FSH, abolished secondary secretion of FSH and hypersecretion of FSH in estrous afternoon. The latter was decreased by LHRHa and abolished by EB or bFF. In contrast, EB induced an hypersecretion of LH in RU486-treated rats at 1800h in estrus.3. It can be concluded that in the absence of the proestrous progesterone actions, the absence of the inhibitory effect of the ovary in estrus evoked a LHRH independent secretion of FSH.     

The induction of divergent gonadotropin secretion in vitro by variations in luteinizing hormone releasing hormone pulse regimen

The effects of luteinizing hormone releasing hormone (LHRH) pulse amplitude, duration, and frequency on divergent gonadotropin secretion were examined using superfused anterior pituitary cells from selected stages of the rat estrous cycle. Cells were stimulated with one of five LHRH regimens. With low-amplitude LHRH pulses (regimen 1) in the presence of potentially estrogenic phenol red, LH response in pituitary cells from proestrus 1900, estrus 0800, and diestrus 1,0800 were all significantly larger (P less than 0.05) than the other stages tested. In the absence of phenol red, responsiveness at proestrus 1900 was significantly larger than proestrus 0800, proestrus 1500, and estrus 0800 (P less than 0.01, 0.05, and 0.05, respectively); other cycle stages tested were smaller. No significant differences were observed between cycle stages for follicle-stimulating hormone (FSH) secretion in the presence or absence of phenol red. Because pituitary cells at proestrus 1900 were the most responsive to low-amplitude 4 ng LHRH pulses, they were also used to study the effects of LHRH pulses of increased amplitude or duration and decreased frequency. Increasing the amplitude (regimen 2) or the duration (regimens 3 to 5) increased FSH secretion; this effect was greatest with regimens 3 and 5. When regimens 3 and 5 were studied in pituitary cells obtained at proestrus 1500, FSH was significantly increased by both regimes, but most by regimen 5; furthermore, LH release was significantly reduced. When regimens 3 and 5 were studied in pituitary cells obtained at estrus 0800, FSH release was elevated most significantly by regimen 5. Thus, variations in LHRH pulse regimen were found to be capable of inducing significant divergence in FSH release from superfused anterior pituitary cells derived from specific stages of the estrous cycle.     

Effects of pulsatile infusion of luteinizing hormone-releasing hormone on luteinizing hormone secretion and ovarian function in hypophysial stalk-transected beef heifers

Hypothalamic regulation of luteinizing hormone (LH) secretion and ovarian function were investigated in beef heifers by infusing LH-releasing hormone (LHRH) in a pulsatile manner (1 microgram/ml; 1 ml during 1 min every h) into the external jugular vein of 10 hypophysial stalk-transected (HST) animals. The heifers were HST approximately 30 mo earlier. All heifers had increased ovarian size during the LHRH infusion. The maximum ovarian size (16 +/- 2.7 cm3) was greater (P less than 0.01) than the initial ovarian size (8 +/- 1.4 cm3). Ovarian follicular growth occurred in 4 of 10 HST heifers in response to pulsatile LHRH infusion. In 2 heifers, an ovarian follicle developed to preovulatory size, but ovulation occurred in only 1 animal after the frequency of LHRH was increased (1 microgram every 20 min during 8 h). In blood samples obtained at 20-min intervals every 5th day, LH concentrations in peripheral serum remained consistently low (0.9 ng/ml) and nonepisodic in the 10 HST heifers during infusion of vehicle on the day before beginning LHRH. In 7 of 10 HST animals, episodic LH secretion occurred in response to pulsatile infusion of LHRH. In 3 of these long-term HST heifers, however, serum LH remained at basal levels and the isolated pituitary seemingly was unresponsive to pulsatile infusion of LHRH as indicated by sequential patterns of gonadotropin secretion obtained at 5-day intervals. These results indicate that pulsatile infusion of LHRH induces LH release in HST beef heifers.     

Anisomycin inhibition of estradiol-induced and progesterone-facilitated luteinizing hormone surges in the immature rat

These studies were designed to examine the effect of anisomycin, a potent and reversible inhibitor of protein synthesis with low systemic toxicity in rodents, on induction of luteinizing hormone (LH) surges by estradiol and their facilitation by progesterone. Immature female rats that received estradiol implants at 0900 h on Day 28 had LH surges approximately 32 h later (1700 h on Day 29). Insertion of progesterone capsules 24 h after estradiol led to premature (by 1400 h) and enhanced LH secretion. Protein synthesis was inhibited by 97%, 95%, 47%, and 16% in the hypothalamus-preoptic area (HPOA) and by 98%, 87%, 35%, and 0% in the pituitary at 30 min, 2 h, 4 h, and 6 h after s.c. injection of anisomycin (10 mg/kg BW), respectively. A single injection of anisomycin at 0, 3, 6, 9, 12, 24, 27, or 30 h after estradiol treatment significantly lowered serum LH levels at 32 h. The effect of injecting anisomycin at 0, 24, or 27 h was overridden by progesterone treatment at 24 h, but LH secretion was delayed serum LH levels were basal (10-30 ng/ml) at 1400 h but elevated (500-800 ng/ml) at 1700 h. Complete suppression of LH surges in estradiol-plus-progesterone-treated rats was achieved with 2 injections of anisomycin on Day 29 at 0900 h and again at 1200 h or 1400 h. Further experiments were designed to examine proteins that might be involved in anisomycin blockade of progesterone-facilitated LH surges. Intrapituitary LH concentrations at 1700 h on Day 29 were 70-80% higher (102 +/- 12.5 micrograms/pituitary) in rats that received 2 injections of anisomycin than in vehicle-treated controls (58.5 +/- 7.7 micrograms/pituitary). There were no significant effects of anisomycin on cytosol progestin receptors in the HPOA (7.1 +/- 1.5 fmol/tissue, anisomycin; 7.2 +/- 0.3, vehicle) or pituitary (8.3 +/- 1.3 fmol/tissue, anisomycin; 11.7 +/- 2.9, vehicle) at this time. The concentration of pituitary gonadotropin-releasing hormone receptors (GnRH-R), however, was significantly lower after anisomycin (265 +/- 30 vs. 365 +/- 37 fmol/mg protein) treatment. These results suggest that both estradiol-induced and progesterone-facilitated LH surges involve protein synthetic steps extending over many hours. Blockade of progesterone-facilitated LH surges by anisomycin appears to be due primarily to an effect on release of LH to which lowering of GnRH-R levels may contribute.     

Effect of luteinizing hormone releasing hormone pulse characteristics on comparative luteinizing hormone and follicle stimulating hormone secretion from superfused rat anterior pituitary cell cultures

We have shown that 4 ng luteinizing hormone releasing hormone (LHRH) pulses induced significantly greater luteinizing hormone (LH) release from proestrous rat superfused anterior pituitary cells with no cycle related differences in follicle stimulating hormone (FSH). Current studies gave 8 ng LHRH in various pulse regimens to study amplitude, duration and frequency effects on LH and FSH secretion from estrous 0800, proestrous 1500 and proestrous 1900 cells. Regimen 1 gave 8 ng LHRH as a single bolus once/h; regimen 2 divided the 8 ng into 3 equal 'minipulses' given at 4 min intervals to extend duration; regimen 3 gave the 3 'minipulses' at 10 min intervals, thereby further extending duration: regimen 4 was the same as regimen 2, except that the 3 'minipulses' were given at a pulse frequency of 2 h rather than 1 h. In experiment 1, all four regimens were employed at proestrus 1900. FSH was significantly elevated by all 8 ng regimens as compared to 4 ng pulses; further, 8 ng divided into 3 equal 'minipulses' separated by 4 min at 1 and 3 h frequencies (regimens 2 and 4) resulted in FSH secretion that was significantly greater than with either a single 8 ng bolus (regimen 1) or when the 'minipulses' were separated by 10 min (regimen 3). In experiment 2, at proestrus 1500, FSH response to the second pulse of regimen 4 was significantly greater than in regimen 2; LH release was significantly suppressed at pulse 2 compared to regimen 2 accentuating divergent FSH secretion. At estrus 0800, FSH response to the second pulse of regimen 4 was significantly stimulated FSH at proestrus 1900, 1500 and estrus 0800, FSH divergence was most marked at proestrus 1500. These data indicate a potential role for hypothalamic LHRH secretory pattern in inducing divergent gonadotropin secretion in the rat.     

Pituitary luteinizing hormone-releasing hormone receptors in ovariectomized cows after challenge with ovarian steroids

Acute changes of bovine pituitary luteinizing hormone-releasing hormone (LHRH) receptors in response to steroid challenges have not been documented. To investigate these changes 96 ovariectomized (OVX) cows were randomly allotted to one of the following treatments: 1) 1 mg estriol (E3); 2) 1 mg 17 beta-estradiol (E2); or 3) 25 mg progesterone (P) twice daily for 7 days before 1 mg E2 and continuing to the end of the experiment. Serum was collected at hourly intervals from 4 animals in each group for 28 h following estrogen treatment. Four animals from each treatment were killed at 4-h intervals from 0 to 28 h after estrogen injection to recover pituitaries and hypothalami. Treatment with E3 or E2 decreased serum luteinizing hormone (LH) within 3 h and was followed by surges of LH that were temporally and quantitatively similar (P greater than 0.05). Progesterone did not block the decline in serum LH, but did prevent (P less than 0.05) the E2-induced surge of LH. Serum follicle-stimulating hormone (FSH) was unaffected (P less than 0.05) by treatment. Pituitary concentrations of LH and FSH were maximal (P less than 0.001) at 16 h for E3 and 20 h for E2, whereas P prevented (P greater than 0.05) the pituitary gonadotropin increase. Concentrations of LHRH in the hypothalamus were similar (P greater than 0.05) among treatments. Pituitary concentrations of receptors for LHRH were maximal (P less than 0.005) 12 h after estrogen injection (approximately 8 h before the LH surge), even in the presence of P. This study demonstrated that in the OVX cow: 1) E2 and E3 increased the concentration of receptors for LHRH and this increase occurred before the surge of LH; and 2) P did not block the E2-induced increase in pituitary receptors for LHRH but did prevent the surge of LH.     

Effects of intraventricular norepinephrine on LH release in short- and long-term ovariectomized steroids-primed rats

This study examined the noradrenergic mechanism in regulation of luteinizing hormone (LH) release in short- and long-term ovariectomized (OVX) steroids-primed rats. All rats were OVX on the diestrous day 1(D1) morning about 1000 h. After OVX, rats in the short-term OVX group were immediately primed with estradiol (E2, 0.1 mg/kg BW s.c.), fitted with atrial Silastic tubing, and a guide cannula in the right lateral cerebroventricle stereotaxically. Rats in the long-term OVX group received the same treatment (E2, atrial tubing and guide cannula implantation) three weeks later. Rats in both groups received progesterone (2 mg/rat s.c.) at 0930 h on the next day after E2. At 1000 h, intraventricular administration of norepinephrine HCl (NE, 0.01, 0.1, or 1.0 microgram in 2 microliters saline) was given. In short-term OVX-steroids-primed rats, NE did not alter LH levels in the peripheral plasma within 60 or 100 min. By contrast, in long-term OVX-steroids-primed rats, 1.0 microgram of NE gradually decreased plasma LH concentrations, which became significantly different from the initial value at the 60 min time point after treatment. On the other hand, intraventricular injection of 5 ng of the LH-releasing hormone (LHRH) elevated plasma LH concentrations within 10 min in both groups of rats, but at different efficacy: a brief release of LH in short-term OVX-steroids-primed rats and a prolonged release of LH in long-term OVX-steroids-primed rats. These results indicated that the interval after OVX plays a critical role in modulating the responsiveness to NE and LHRH in the steroids-primed OVX rats.     

Effect of luteinizing hormone releasing hormone (LHRH) and [D-Trp6, des-Gly-NH2(10)]LHRH ethylamide on alpha-subunit and LH beta messenger ribonucleic acid levels in rat anterior pituitary cells in culture

The effect of incubation with LHRH and its agonist [D-Trp6, des-Gly-NH2(10)]LHRH ethylamide has been measured on the concentrations of mRNAs for the common alpha-subunit of glycoprotein hormones and beta-LH in rat anterior pituitary cells in primary culture. After incubation, total RNA was analyzed by Northern blot or dot blot hybridization with alpha- and LH beta 32P-labeled cRNA probes and mRNA levels were quantified by autoradiography. Short-term treatment (4-6 h) of pituitary cells with 100 nM LHRH led to a marked stimulation of LH release but no effect was observed on alpha-subunit or LH beta mRNA levels. Longer (24-72 h) incubation periods with LHRH led to complete desensitization of the LH response to the neurohormone and induced 2- to 3-fold increases in alpha-mRNA cell content while LH beta mRNA levels remained unchanged. Maximal induction of alpha mRNA accumulation was observed with an LHRH concentration as low as 0.1 nM. Incubation with the LHRH agonist [D-Trp6, des-Gly-NH2(10)]LHRH ethylamide for 24-72 h also increased alpha mRNA but did not modify LH-beta mRNA levels. It is concluded that long-term exposure of anterior pituitary cells to LHRH or to an LHRH agonist positively regulates alpha-subunit gene expression in the absence of change in LH beta mRNA levels. This observation can provide an explanation for the high plasma levels of free alpha-subunits found in patients treated chronically with LHRH agonists.     

An acute increase in serum prolactin does not modify gonadotropin release in female rats

Attempts were made to find out whether hyperprolactinemia has an effect on the hypothalamo-pituitary response to estrogen feedback and LHRH stimulation. Adult female rats of Wistar strain were ovariectomized and received subcutaneous injection of 20 micrograms estradiol benzoate (EB) 3-4 weeks later (day-0). A second injection of 20 micrograms EB, when administered at noon on day-3, induced a highly significant increase in serum LH (p less than 0.001 vs. basal values), but not FSH, estimated at 1800 h on the same day. This EB-promoted LH release was not altered by pretreatment with rat PRL (5 micrograms/day), which was administered subcutaneously daily in the morning (1100 h) between day-1 and day-3. No statistical difference in the serum LH concentration was found when compared with the values for the control animals pretreated with 0.9% saline alone. Serum gonadotropins 15 min after LHRH administration (100 ng/100 g BW) in 32-day-old female rats were not statistically different between the animals pretreated with 5 micrograms PRL, which was given subcutaneously daily (at 0800 h) for 3 days, and the controls pretreated with 0.9% saline. These results suggest that an acute increase in serum PRL may not exert a negative effect on the gonadotropin release induced by estrogen feedback and LHRH stimulation.     

Sensitivity differences in reproductive/endocrine organs to chronically administered LHRH agonists in female rats

The acute and chronic effects of two LHRH agonists on reproductive endocrine target organs were examined in female rats. Animals were injected twice daily with [(ImBzl)-D-His6,Pro9-NEt]LHRH (histrelin) or [D-Trp6,Pro9-NEt]LHRH for 1, 3, 5, 7, 11 or 28 days at 1, 10, 100 or 1000 micrograms/kg/day beginning in the luteal phase. The responses observed with the two agonists were similar. An initial stimulatory phase was observed on the first day of treatment with substantial increases in serum LH and progesterone levels. A significant diminution of hormone response was seen by day 3. Only 1000 micrograms/kg abolished the pituitary LH response at later treatment periods. Estrous cyclicity, ovarian and uterine weight, and progesterone and estradiol levels were inhibited in a time and dose dependent manner. The results demonstrate target organ sensitivity differences. In contrast to the relatively high doses needed to inhibit the pituitary response and decrease ovarian weight, doses as low as 1 microgram/kg were sufficient to decrease uterine weight. If these findings extrapolate to humans, it may be that conditions in which the desired therapeutic action is suppression of uterine tissue, may be treated with lower doses of LHRH agonists than conditions requiring complete gonadal suppression.     

Changes in luteinizing hormone-releasing hormone content of discrete hypothalamic areas associated with spontaneous and induced preovulatory luteinizing hormone surges in the domestic hen

It is widely assumed that luteinizing hormone-releasing hormone (LHRH) neuronal activation is involved in the preovulatory surge of LH in the hen. In addition, this LH surge may be initiated by ovarian progesterone (P4) release. Thus, spontaneous and P4-induced LH surges should be associated with acute changes in LHRH content of discrete hypothalamic areas associated with LHRH cell bodies and/or LHRH axon terminals. Medial preoptic area (mPOA) and infundibulum (INF) LHRH content was measured by radioimmunoassay at intervals before, at, and following peak LH levels of a spontaneous preovulatory surge of LH, as well as when this surge was advanced by P4 administration in laying hens. Nonlaying birds served as additional controls. Levels of serum LH, P4, 17 beta-estradiol and pituitary LH were also measured. Increased (P less than 0.05) LHRH content in mPOA without changes in the INF are associated with peak serum LH levels of the spontaneous LH surge. By contrast, decreased (P less than 0.05) LHRH content in both mPOA and INF is associated with peak serum LH levels when the spontaneous surge was advanced 8 h by P4 administration to laying hens. Medial preoptic area and INF LHRH contents were significantly lower (P less than 0.05) in nonlaying than in laying hens.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of hypothalamic neurohormones on prolactin release from pituitary allografts in the hamster

Recent reports indicate that luteinizing hormone-releasing hormone (LHRH) releases prolactin (PRL) under some circumstances. We examined the chronic effects of LHRH, growth hormone-releasing hormone (GHRH), and corticotrophin-releasing hormone (CRH) on the release of PRL, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) by pituitary allografts in hypophysectomized, orchidectomized hamsters. Entire pituitary glands removed from 7-week-old-male Golden Syrian hamsters were placed under the renal capsule of hypophysectomized, orchidectomized 12-week-old hamsters. Beginning 6 days postgrafting, hamsters were injected subcutaneously twice daily with 1 microgram LHRH, 4 micrograms GHRH, or 4 micrograms CRH in 100 microliter of vehicle for 16 days. Six hosts from each of the four groups were decapitated on Day 17, 16 hr after the last injection. Prolactin, LH, and FSH were measured in serum collected from the trunk blood. Treatment with LHRH significantly elevated serum PRL levels above those measured in the other three groups, which were all similar to one another. Serum LH levels in hosts treated with vehicle were elevated above those measured in the other three groups. Serum FSH levels in hosts treated with LHRH were greater than FSH levels in any of the other three groups. These results indicate that chronic treatment with LHRH can stimulate PRL and FSH release by ectopic pituitary cells in the hamster.     

Effect of bombesin on basal and stimulated secretion of some pituitary hormones in humans

The effect of bombesin (5 ng/kg/min X 2.5 h) on basal pituitary secretion as well as on the response to thyrotropin releasing hormone (TRH; 200 micrograms) plus luteinizing hormone releasing hormone (LHRH; 100 micrograms) was studied in healthy male volunteers. The peptide did not change the basal level of growth hormone (GH), prolactin, thyroid-stimulating hormone (TSH), luteinizing hormone (LH) and follicle-stimulating hormone (FSH). On the contrary, the pituitary response to releasing hormones was modified by bombesin administration. When compared with control (saline) values, prolactin and TSH levels after TRH were lower during bombesin infusion, whereas LH and FSH levels after LHRH were higher. Thus bombesin affects in man, as in experimental animals, the secretion of some pituitary hormones.