EFFECTS OF GnRH ON LUTEINIZING HORMONE RELEASE AND ONSET OF CYCLIC OVARIAN ACTIVITY POSTPARTUM IN PELIBUEY EWES

1988 ◽  
Vol 68 (2) ◽  
pp. 359-366 ◽  
Author(s):  
A. GONZALEZ R. ◽  
B. D. MURPHY
Keyword(s):  
Luteinizing Hormone ◽  
Key Words ◽  
Luteal Phase ◽  
Gonadotropin Releasing Hormone ◽  
Ovarian Activity ◽  
Hormone Release ◽  
Similar Magnitude ◽  
Hair Sheep ◽  
Peripheral Plasma ◽  
Lh Release

Synthetic gonadotropin releasing hormone (GnRH) was administered to Pelibuey ewes to determine its effect on luteinizing hormone (LH) release and on cyclic ovarian activity during the first 3 – 4 wk postpartum. Two GnRH doses were given (10 and 100 μg) on days 4 and 5, 7 and 8, 14 and 15, and 21 and 22, after parturition, respectively. In three trials, 11, 8 and 7 ewes were used. For each trial 5, 3 and 2 ewes were used as controls, respectively; in trial 3, only the 100-μg dose was given once. Results from the three trials indicated that LH release always occurred after GnRH treatment, relative to the saline-treated controls. In trials 1 and 2, the 10-μg dose induced a higher (P < 0.001) LH release than the 100-μg dose; the LH release in response to the 100-μg dose in the three trials was of similar magnitude. Release of LH in response to both doses was lower (P < 0.05) during days 4 – 5 postpartum, than during the following 3 wk. Two types of luteal activity or steroidogenesis were observed in the GnRH-treated ewes, relative to the saline-treated ewes; (1) within 2 – 4 d after each GnRH injection small peaks of progesterone appeared, and (2) within 5 – 15 d after the last GnRH injection there were elevations of progesterone in peripheral plasma to concentrations and of durations characteristic of the luteal phase of the ovine estrous cycle. These results indicate that the pituitary of postpartum Pelibuey ewes regains the ability for maximal release of LH in response to GnRH challenge within 7 d postpartum. Further, treatment with GnRH induces earlier return to cyclic ovarian activity. Key words: Hair sheep, postpartum, GnRH, luteal activity

Role of Ca2+ and Na+ on luteinizing hormone release from the calf pituitary

1988 ◽  
Vol 255 (4) ◽  
pp. E469-E474
Author(s):  
J. P. Kile ◽  
M. S. Amoss
Keyword(s):  
Luteinizing Hormone ◽  
Ionophore A23187 ◽  
Channel Blockers ◽  
Hormone Release ◽  
Primary Cells ◽  
Rat Pituitary ◽  
Voltage Dependent ◽  
Lh Release ◽  
Ca2 Channels

It has been proposed that gonadotropin-releasing hormone (GnRH) stimulates Ca2+ entry by activation of voltage-independent, receptor-mediated Ca2+ channels in the rat gonadotroph. Little work has been done on the role of calcium in GnRH-induced luteinizing hormone (LH) release in species other than the rat. Therefore, this study was done to compare the effects of agents that alter Ca2+ or Na+ entry on LH release from calf anterior pituitary primary cells in culture. GnRH (100 ng/ml), Ca2+ ionophore A23187 (2.5 microM), and the depolarizing agent ouabain (0.1-10 microM) all produced significant increases (P less than 0.05) in LH release; these effects were significantly reduced when the cells were preincubated with the organic Ca2+ channel blockers nifedipine (1-10 microM) and verapamil (1-10 microM) and with Co2+ (0.01-1 mM). The effect of ouabain was inhibited by tetrodotoxin (TTX; 1-10 nM) as well as by nifedipine at 0.1-10 microM. In contrast to its effect on rat pituitary LH release, TTX significantly inhibited GnRH-stimulated LH release at 1-100 nM. These results suggest that GnRH-induced LH release may employ Ca2+ as a second messenger in bovine gonadotrophs and support recent speculation that GnRH-induced Ca2+ mobilization may in part be voltage dependent.

RELATIONSHIP BETWEEN BLOOD LEVELS OF LUTEINIZING HORMONE AND TESTOSTERONE IN BULLS, AND THE EFFECTS OF SEXUAL STIMULATION

1971 ◽  
Vol 50 (3) ◽  
pp. 457-466 ◽  
Author(s):  
C. B. KATONGOLE ◽  
F. NAFTOLIN ◽  
R. V. SHORT
Keyword(s):  
Luteinizing Hormone ◽  
Immediate Release ◽  
Blood Levels ◽  
Testosterone Levels ◽  
Peripheral Plasma ◽  
Sexual Stimulation ◽  
Maximal Stimulation ◽  
Cyclical Pattern ◽  
Lh Release ◽  
Competitive Protein Binding

SUMMARY Luteinizing hormone (LH) and testosterone were measured in the peripheral plasma of two bulls by radioimmunoassay and competitive protein binding techniques. Samples were collected from an indwelling jugular catheter once an hour for 24 h, and then at more frequent intervals after a number of experimental procedures. Each bull showed its own characteristic pattern of cyclic LH changes, with 5–10 peaks during 24 h that were apparently unrelated to daylight, feeding or sleep. Each LH peak was associated with a testosterone peak; the LH concentrations ranged from 5 to 50 ng/ml, and those of testosterone from 2 to 20 ng/ml. Sexual stimulation, such as the sight of a cow, or 'teasing', or on one occasion the act of ejaculation itself, caused an immediate release of a large amount of LH. If the testosterone levels were low at the time, the LH peak was followed by a testosterone peak. But when the testosterone levels were high at the time of LH discharge, the testis seemed to be unable to respond any further. An intravenous injection of 500 i.u. human chorionic gonadotrophin was associated with LH release and caused the testosterone levels to rise to maximal values of 22 ng/ml within 1½ h. It is concluded that the cyclical pattern of LH release is due to some inherent central rhythm, and that each transient LH peak results in transient maximal stimulation of testicular testosterone secretion.

scholarly journals Effect of androgen on Kiss1 expression and luteinizing hormone release in female rats

2017 ◽  
Vol 233 (3) ◽  
pp. 281-292 ◽  
Author(s):  
Kinuyo Iwata ◽  
Yuyu Kunimura ◽  
Keisuke Matsumoto ◽  
Hitoshi Ozawa
Keyword(s):  
Luteinizing Hormone ◽  
Arcuate Nucleus ◽  
Female Rats ◽  
Hormone Release ◽  
Lh Surge ◽  
Continuous Release ◽  
Ovulatory Dysfunction ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion

Hyperandrogenic women have various grades of ovulatory dysfunction, which lead to infertility. The purpose of this study was to determine whether chronic exposure to androgen affects the expression of kisspeptin (ovulation and follicle development regulator) or release of luteinizing hormone (LH) in female rats. Weaned females were subcutaneously implanted with 90-day continuous-release pellets of 5α-dihydrotestosterone (DHT) and studied after 10 weeks of age. Number of Kiss1-expressing cells in both the anteroventral periventricular nucleus (AVPV) and arcuate nucleus (ARC) was significantly decreased in ovary-intact DHT rats. Further, an estradiol-induced LH surge was not detected in DHT rats, even though significant differences were not observed between DHT and non-DHT rats with regard to number of AVPV Kiss1-expressing cells or gonadotrophin-releasing hormone (GnRH)-immunoreactive (ir) cells in the presence of high estradiol. Kiss1-expressing and neurokinin B-ir cells were significantly decreased in the ARC of ovariectomized (OVX) DHT rats compared with OVX non-DHT rats; pulsatile LH secretion was also suppressed in these animals. Central injection of kisspeptin-10 or intravenous injection of a GnRH agonist did not affect the LH release in DHT rats. Notably, ARC Kiss1-expressing cells expressed androgen receptors (ARs) in female rats, whereas only a few Kiss1-expressing cells expressed ARs in the AVPV. Collectively, our results suggest excessive androgen suppresses LH surge and pulsatile LH secretion by inhibiting kisspeptin expression in the ARC and disruption at the pituitary level, whereas AVPV kisspeptin neurons appear to be directly unaffected by androgen. Hence, hyperandrogenemia may adversely affect ARC kisspeptin neurons, resulting in anovulation and menstrual irregularities.

Melatonin inhibition of GnRH-induced LH release from neonatal rat gonadotroph: involvement of Ca2+ not cAMP

1995 ◽  
Vol 269 (1) ◽  
pp. E85-E90 ◽  
Author(s):  
J. Vanecek ◽  
D. C. Klein
Keyword(s):  
Luteinizing Hormone ◽  
Second Messenger ◽  
Gonadotropin Releasing Hormone ◽  
Neonatal Rat ◽  
Dibutyryl Camp ◽  
Releasing Hormone ◽  
Cyclic Monophosphate ◽  
Lh Release

Melatonin inhibits gonadotropin-releasing hormone-induced release of luteinizing hormone (LH) from the neonatal rat gonadotrophs. The second messenger involved is not known, although there are several candidates, including adenosine 3',5'-cyclic monophosphate (cAMP) and intracellular free Ca2+. The present study addresses the question of which second messenger mediates melatonin inhibition of LH release. We found that the effect of melatonin was not prevented by cAMP protagonists, including 8-bromo-cAMP, dibutyryl cAMP, 3-isobutyl-1-methylxanthine, and forskolin. However, treatments that enhanced Ca2+ influx masked the effects of melatonin, and treatments that blocked Ca2+ influx mimicked the effects of melatonin. Moreover, melatonin decreased K(+)-induced LH release, which is dependent on Ca2+ influx but did not block release of LH due to thapsigargin-induced mobilization of Ca2+ from intracellular stores. These findings indicate that melatonin inhibits gonadotropin-releasing hormone-induced LH release, primarily through an action involving inhibition of Ca2+ influx, and that cAMP does not seem to be involved in this effect of melatonin.

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