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PubMed1982

Effects of chronic treatment with a potent luteinizing hormone releasing hormone agonist on serum luteinizing hormone and steroid levels in the male rhesus monkey.

The effects of chronic administration of [D-Ser(TBU)6, des-Gly-NH2 10]LHRH ethylamide (Buserelin, Hoe 766) on plasma LH, pregnenolone, 17-hydroxyprogesterone, testosterone and dihydrotestosterone levels were studied in a nonhuman primate species, the rhesus monkey. After 1 week of daily administration of 25 micrograms of Hoe 766, the LH response measured after 3 h and 7 h is markedly inhibited when compared to the previous week's response and a slight decrease in basal LH levels is observed. A small rise of plasma LH is, however, always seen 3 h after administration of the peptide during the whole treatment period. Serum testosterone levels display a rapid stimulation from 7 to 35 ng/ml 3 h after the first administration of Buserelin and increase progressively up to at least 12 h (44 ng/ml). Plasma concentrations of 17-hydroxyprogesterone increase more slowly from 2.0 to 3.4 ng/ml during the first 3 h and reach 9.5 ng/ml 9 h later. By contrast, there are no or minimal changes or serum pregnenolone and dihydrotestosterone levels following the first injection of Hoe 766 and during the course of the study. While the acute testosterone response to Buserelin measured at 3 h is not affected in up to seven weeks of treatment with the peptide, the duration of testosterone and 17-hydroxyprogesterone response measured at later time intervals (7 h, 12 h) is decreased to 20% to 50% of control. The data suggest that the testicular steroidogenic pathway in rhesus monkeys retain its ability to respond to LH stimulation during treatment with the LHRH agonist while the basal testosterone levels are reduced. The close correlation observed between reduced serum LH and testosterone concentrations suggest that pituitary desensitization is the main factor responsible for the partial inhibition of basal testosterone concentration in rhesus monkeys.

Animals↗
PubMed1995

Regulation of luteinizing hormone-releasing hormone (LHRH) secretion by melatonin in the ewe. I. Simultaneous delayed increase in LHRH and luteinizing hormone pulsatile secretion.

This study was performed to test the hypothesis that a short-day-like melatonin treatment would induce simultaneous stimulations of LHRH and LH secretion. Simultaneous serial samples of jugular and portal blood to assay LH and LHRH, respectively, were carried out at three different periods according to the expected changes in LH secretion. Twenty-six ovariectomized ewes bearing a subcutaneous implant of estradiol and exposed to a long-day photoperiod (16L:8D) received s.c. implants of melatonin on Day 0. LHRH and LH pulsatile secretion was studied in the first group during inhibition of LH secretion by long days (on Day -1, n = 6). A second group (n = 9) was sampled on Day 39. Moreover, seven animals from this group were sampled on Day 46 to focus on the beginning of LH increase. The third group (n = 6) was sampled during maximal LH secretion (Day 74, n = 6). A fourth group (n = 5) composed of noncannulated animals was sampled for LH secretion only as a control for the effects of surgical procedures. On each occasion, blood was collected every 10 min for 6 h. Between Day -1 and Day 39, LHRH pulse frequency was low and did not differ. In the same animals, this value became 2.5-fold higher between Day 39 and Day 46. Finally, on Day 74, LHRH pulse frequency was about 6-fold higher than on Day -1.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1995

Regulation of luteinizing hormone-releasing hormone (LHRH) secretion by melatonin in the ewe. II. Changes in N-methyl-D,L-aspartic acid-induced LHRH release during the stimulation of luteinizing hormone secretion by melatonin.

Injection of N-methyl-D,L-aspartic acid (NMDA), a glutamatergic agonist, cause an acute release of LH. The amount of LH released is modulated by photoperiod in sheep; it is larger in animals in which reproductive activity has been inhibited by long days than in those photostimulated by short days. The purpose of the present experiment was to determine whether this effect of photoperiod on LH response to NMDA is mediated by melatonin and whether it reflects a change in the amount of LHRH released in response to NMDA. Twenty-one ovariectomized ewes, bearing an s.c. implant of estradiol and kept in long days (16L:8D), received s.c. implants of melatonin on Day 0. The effect of a single injection of NMDA (5 mg/kg i.v.) on LHRH and simultaneous LH secretion was studied at three different periods of the stimulation of LH secretion by the melatonin treatment: first, during inhibition of LH secretion by long days (on Day -1, n = 6); secondly, during the onset of the LH increase (on Day 39, n = 9); and thirdly, during maximum LH secretion (on Day 74, n = 6). The stimulation of LHRH secretion by administration of NMDA was characterized by a large and long increase in LHRH concentration on Day -1 and Day 39. There was no significant difference between these two periods in terms of duration and amplitude of the LHRH release. On Day 74, the stimulation was much shorter than on Day -1 and Day 39 and was followed by a phase of decreased pulsatility of LHRH secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1996

Suppression in the secretion of follicle-stimulating hormone and luteinizing hormone, and ovarian follicle development in heifers continuously infused with a gonadotropin-releasing hormone agonist.

A novel experimental model was developed in cattle to investigate the requirement for FSH and LH during ovarian follicle growth and development. On Day 5 of the estrous cycle, 7 heifers were each implanted with an osmotic minipump containing a GnRH agonist (GnRHa), Buserelin (release rate, 2.5 micrograms/h). Another 7 heifers served as controls. Each minipump was replaced 28 days later with a second pump, which was left in place for a further 20 days. Blood samples were collected daily throughout the experimental period, and frequent samples were also collected on both days of minipump insertion and at 10 days after insertion of the second pump. The ovaries of all heifers were scanned daily by real-time ultrasonography to monitor follicular dynamics. All controls displayed 2 or 3 waves of FSH and follicular development per estrous cycle during the experiment. Insertion of the first minipump produced a large LH and FSH surge and induced ovulation in all 7 animals. Within 8 days of the start of treatment, serum LH concentrations fell to basal levels; they then remained constant at this level throughout the infusion period, only beginning to recover 4-5 days after the termination of infusion. After the initial increase, FSH returned to basal levels before showing a normal wave that was coincident with the emergence, growth, and regression of a dominant follicle. However, despite the peak levels of FSH, dominant follicles from the next wave failed to grow beyond 7-9 mm; they remained at this size for 3 wk until 3-4 days after insertion of the second minipump, when FSH fell precipitously to reach low levels that were maintained throughout the remainder of the infusion. After this fall in FSH concentrations, these follicles regressed rapidly, and no antral follicles > 4 mm were detected until after the termination of treatment. Thereafter, FSH concentrations increased significantly; the increase was accompanied by the emergence of a follicular wave and development of a dominant follicle, with estrus observed 8-11 days later. In conclusion, this study has demonstrated clearly that in cattle the early stages of follicle development (< or = 4 mm) are not dependent on acute support by gonadotropins. However, FSH is required for further growth of follicles up to 9 mm, while LH pulses are indispensable for follicle development beyond 9 mm in diameter. The model developed in this study should be valuable for studying the control of ovarian follicle development and atresia in vivo.

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PubMed1998

Expression of Fos within luteinizing hormone-releasing hormone neurons, in relation to the steroid-induced luteinizing hormone surge in guinea pigs.

The induction of Fos protein was examined within LHRH neurons of guinea pigs; the aim was to delineate relationships between subgroups of LHRH neurons during an LH surge in a laboratory rodent in which the distribution of LHRH neurons and the presence of a true luteal phase in the reproductive cycle resemble those in primates. Approximately one third of the forebrain population of LHRH neurons was examined in ovariectomized steroid-treated guinea pigs killed either before or during a steroid-induced LH surge. LHRH/Fos double-labeled neurons were more abundant in surging compared to presurge guinea pigs (p = 0.008) and were most abundant within the preoptic area and anterior hypothalamus. Nonetheless, double-labeled LHRH/Fos neurons were observed throughout the remainder of the population of LHRH neurons in surging guinea pigs. A relative loss of LHRH reaction product was detected by image analysis in the LHRH terminals in the median eminence of surging guinea pigs, consistent with augmented LHRH release. Thus, there appears to be a coordinated increase in Fos expression in subgroups of LHRH neurons, more pronounced in rostral, as compared to caudal, regions in guinea pigs killed after the peak of the steroid-induced LH surge.

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PubMed1998

Fos expression in luteinizing hormone-releasing hormone neurons of guinea pigs, with knife cuts separating the preoptic area and the hypothalamus, demonstrating luteinizing hormone surges.

LHRH neurons in guinea pigs, as in primates and other non-rodent species, are broadly distributed in the basal forebrain. In this study, knife cuts were made in the anterior hypothalamus, effectively separating more caudally positioned hypothalamic LHRH neurons from those in rostral preoptic areas. Guinea pigs with knife cuts displayed an LH surge in response to steroid administration. There was no significant difference in the number of LHRH neurons that expressed Fos in conjunction with an LH surge, although fewer total LHRH neurons were detected in the forebrain of knife-cut versus sham-cut animals. Knife-cut animals displayed a larger percentage of LHRH/Fos neurons in one region of the caudal hypothalamus than sham-cut animals. The area and perimeter of the LHRH reaction product within the cytoplasm of LHRH/Fos neurons were smaller than those of single-labeled LHRH neurons in sham-cut animals and in the caudal hypothalamus, but not the rostral preoptic area, of knife-cut animals. We conclude that caudal hypothalamic LHRH neurons separated from rostral preoptic regions are capable of sustaining an LH surge in guinea pigs. This finding is important, as LHRH neurons are present in the caudal hypothalamus, as well as in preoptic areas, of a large number of mammalian species, including humans.

Animals↗
PubMed1987

Morphological evidence that luteinizing hormone-releasing hormone neurons participate in the suppression by estradiol of pituitary luteinizing hormone secretion in ovariectomized rats.

Morphological characteristics of LHRH neurons identified by immunocytochemistry were studied using light and electron microscopy in female rats in which estradiol was replaced at the time of ovariectomy ('pseudo-intact' rats) or 3 weeks after ovariectomy (long-term ovariectomized, estradiol-treated). While estradiol levels were equivalent in these two groups, the rise in LH after ovariectomy was prevented by the immediate administration in the pseudo-intact rats, while the augmented plasma LH levels present three weeks following ovariectomy were only reduced by 50% as a result of delayed estradiol treatment. The LHRH content of the medial basal hypothalamus (MBH) including the median eminence (ME) was greater in pseudo-intact females than in untreated long-term ovariectomized control females or long-term ovariectomized, estradiol-treated females, both 1 and 14 days after estradiol exposure. Immunocytochemistry revealed fewer LHRH-immunopositive neuronal processes coursing throughout the MBH and terminating in the ME of long-term ovariectomized, estradiol-treated rats compared to those in pseudo-intact rats. However, within individual neurovascular terminals in the ME, image analysis revealed that the area of reaction product was greater in long-term ovariectomized, estradiol-treated animals. Equivalent amounts of LHRH were assayed in the MBH within each group of animals by several LHRH antisera regardless of their different binding requirements (R42, IJ29 and A-R743), suggesting that the predominant moiety present in neuronal terminals is the fully mature decapeptide. In contrast, in the preoptic area-anterior hypothalamus (POA-AH) these antisera assayed amounts of LHRH that varied as a function of binding characteristics, although the quantities did not vary with the estradiol treatment schedule. Immunocytochemical results paralleled these assay data; antisera requiring an interior sequence of amino acids (A-R743 and A-R419) detected approximately 3 times as many immunoreactive perikarya in the POA-AH as did an antiserum requiring the free amidated C terminal (IJ29). The estradiol treatment schedules had no effect on the total number of LHRH-immunopositive neurons detected by each antiserum or the distribution of LHRH-immunopositive neuronal perikarya. These data support the hypothesis that the predominant moieties present in neuronal cell bodies are precursor forms. The fine-structural characteristics of LHRH-immunopositive neuronal cell bodies are consistent with greater secretory and biosynthetic activity in LHRH neurons of long-term ovariectomized, estradiol-treated rats.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

A self-priming effect of luteinizing hormone releasing hormone on follicle-stimulating hormone secretion in the adult male rat.

In order to determine whether male rats show a self-priming effect of LHRH on FSH secretion, young adult male rats were anesthetized with ketamine HCl and injected intravenously with 50 ng LHRH/100 g body weight at 30- or 60-min intervals. Blood samples were collected by heart puncture and analyzed for FSH by radioimmunoassay. Animals injected at 30-min intervals released more FSH in response to the third and fourth injection than in response to the first. Castration 4 days prior to testing eliminated this response. Treatment of castrated male rats with a testosterone-filled Silastic capsule large enough to maintain secondary sexual organ weights and serum FSH concentrations at levels similar to those found in intact animals maintained the response. A smaller testosterone capsule did not. These data indicate that a self-priming effect of LHRH on FSH secretion exists in the adult male rat. This response requires something from the testes, probably testosterone, for its maintenance.

Animals↗
PubMed1997

Identification of growth hormone-releasing hormone and somatostatin neurons projecting to the median eminence in normal and growth hormone-deficient Ames dwarf mice.

In the spontaneous mutant Ames dwarf mouse, GH deficiency coincides with a dramatic increase in the expression of both mRNA and peptide for stimulatory GHRH and reduced expression of GH-inhibitory somatostatin (SRIH) mRNA and peptide. However, both GHRH and SRIH are markedly reduced in the dwarf median eminence (ME), suggesting that ME innervation by GHRH and SRIH neurons may be aberrant in the absence of GH. In order to test this hypothesis, the number of GHRH and SRIH ME-projecting neurons was evaluated in normal and dwarf mice using a combination of retrograde tract-tracing and neuron phenotype identification by immunocytochemistry (ICC). Adult animals were injected intraperitoneally with the fluorescent tract-tracer fluorogold (FG), which, in the brain, is taken up only by axons terminating in areas deprived of the blood-brain barrier, such as the ME. Visualization of FG was achieved by either UV illumination or ICC, and was combined as appropriate with fluorescence or bright-field ICC for GHRH or SRIH. Cells immunoreactive for GHRH or SRIH and labeled with FG were quantified at each 180-microns rostral-to-caudal level through the hypothalamus. As reported previously, the total number of hypophysiotropic GHRH neurons was markedly increased in dwarf compared with that in normal mice. However, a similar percentage of ME-innervating GHRH cells was estimated in dwarf (73 +/- 4%) and normal (76 +/- 3%) animals. Such a percentage in dwarfs thus represents a larger population of ME-projecting GHRH cells (749 +/- 53) than in normal mice (128 +/- 15). Increased numbers of FG-labeled GHRH neurons in dwarfs were located at the middle and posterior levels of the arcuate nucleus (2.08, 2.26 and 2.44 mm posterior to bregma). The percentage of FG-labeled SRIH neurons was also similar for dwarf (83 +/- 2%) and normal (87 +/- 2%) mice. Because the total SRIH-immunoreactive neuronal population in dwarfs is significantly reduced compared to that in normal animals, the similar FG-labeled percentage reflects a reduced number of SRIH cells projecting to ME in dwarf (1,376 +/- 104) compared with normal (3,192 +/- 267) mice. Fewer FG-labeled SRIH cells were found in dwarfs at every anterior-to-posterior level of the periventricular nucleus (p < 0.01 for comparisons at 0.28, 0.46, 0.64, and 1.0, and p < 0.05 for comparison at 1.18 mm posterior to the bregma). The present study indicates that the reduction in GHRH and SRIH immunoreactivity in the dwarf ME may result from different phenomena for each neuronal population. The reduction in GHRH immunostaining in the ME, despite a marked increase in the total ME-projecting GHRH neurons, may be interpreted as increased GHRH release, with consequent depletion of the ME stores. In contrast, the deficit in ME SRIH may be proportional to the deficit in the number of detectable SRIH periventricular nucleus neurons.

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