LH responses to LHRH, DBcAMP, and 17 beta-estradiol in cultures derived from aged rats

1981 ◽  
Vol 240 (5) ◽  
pp. E510-E518
Author(s):  
L. K. Tang ◽  
F. Y. Tang
Keyword(s):  
Luteinizing Hormone ◽  
Control Level ◽  
Female Rats ◽  
Female Rat ◽  
Aged Rats ◽  
Luteinizing Hormone Releasing Hormone ◽  
Cyclic Monophosphate ◽  
Fischer 344 ◽  
Lh Release ◽  
Old Rats

Effects of luteinizing hormone-releasing hormone (LHRH), N6,O2'-dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAmP), and 17 beta-estradiol (E2) on LH responses were compared in 4-day-old pituitary cultures derived from female rats (Fischer 344) of 9 and 31 mo of age. Pituitary LH contents were similar in 5 X 10(5) freshly dispersed cells prepared from the two groups of rats. LH release in response to a 4-h incubation with 10 nM LHRH was virtually the same in cultures derived from 9- and 31-mo-old rats, 140 +/- 2 ng and 138 +/- 18 ng/4 h, respectively. In cultures derived from 9-mo-old rats, incubation with 8 mM DBcAMP for 4 h significantly stimulated LH release (286% of control level), and treatment with 10 nM E2 for 3 days significantly increased both basal LH release and LH accumulation (sum of LH contents in cells and medium) to 162 and 125% of control level, respectively. Neither DBcAMP nor E2 affected cultures derived from the 31-mo-old rats. These results indicate that there is a difference in the LH response to DBcAMP and E2 between cultures derived from 9- and 31-mo-old rats. The loss of pituitary responsiveness to DBcAMP and E2 and the loss of pituitary cyclicity in the aged female rat may be causally related.

Sex difference in LH response to LHRH and DBcAMP and effect of testosterone.

1978 ◽  
Vol 235 (3) ◽  
pp. E291
Author(s):  
L K Tang
Keyword(s):  
Luteinizing Hormone ◽  
Sex Difference ◽  
Female Rats ◽  
Male Rats ◽  
Camp Production ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Release

Because luteinizing hormone-releasing hormone (LHRH) stimulates both pituitary cAMP production and LH release, cAMP has been implicated in the action of LHRH on LH release. The effects of LHRH and DBcAMP on LH release were tested in 4-h incubations with pituitary cultures prepared from male or female rats. LH contents in medium and cells were separately determined by radioimmunoassays. LH release in response to 10 nM LHRH was significantly greater in cultures prepared from female rats (female-RPC) than in cultures prepared from male rats (male-RPC), 1,070 and 418% of control, respectively. Addition of DBcAMP (3, 5, or 10 mM) significantly stimulated LH release by female-RPC (212, 206, or 286% of control, respectively) but did not affect LH release in male-RPC. Furthermore, DBcAMP significantly increased the cellular LH content in female- but not in male-RPC. Testosterone pretreatment of female-RPC significantly lowered the LHRH-induced LH release but did not affect the DBcAMP-induced LH release. These data indicate that testosterone may contribute to the sex difference in pituitary LH response to LHRH but not to DBcAMP.

Effect of serum sex steroids on pituitary LH response to LHRH and LH synthesis

1980 ◽  
Vol 238 (5) ◽  
pp. E458-E462
Author(s):  
L. K. Tang
Keyword(s):  
Luteinizing Hormone ◽  
Sex Difference ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Male Rat ◽  
Female Rat ◽  
Rat Serum ◽  
Lh Release ◽  
Lh Cells ◽  
Stimulatory Factor

To determine the factors responsible for the sex difference in luteinizing hormone (LH) response to luteinizing hormone-releasing hormone (LHRH) observed earlier in pituitary cultures, we examined the effects of serum, 17 beta-estradiol, and testosterone on pituitary LHRH-responsiveness and LH synthesis. Cultures prepared from female rats were maintained in medium supplemented with serums. Dextran-coated charcoal (DCC) adsorption of female rat serum reduced, whereas DCC adsorption of male rat serum increased the pituitary LHRH-responsiveness, indicating the existence of stimulatory factor(s) in female rat serum and inhibitory factor(s) in male rat serum. Readdition of testosterone to DCC female rat serum significantly reduced LH release in response to LHRH (78-32% of the control) without affecting total LH content. Readdition of 17 beta-estradiol to DCC female rat serum significantly increased the LH release in response to LHRH, cellular LH content, and 3H-labeled precursor uptake and incorporation into immunoprecipitable LH. These results indicate that the sex difference in LHRH responsiveness may be attributed to the stimulatory effect of 17 beta-estradiol and the inhibitory effect of testosterone on the LH cells.

Melatonin inhibits luteinizing hormone releasing hormone (LHRH) induction of LH release from fetal rat pituitary cells

1995 ◽  
Vol 184 (2) ◽  
pp. 109-112 ◽  
Author(s):  
Atsuhiko Hattori ◽  
Damon C. Herbert ◽  
Mary K. Vaughan ◽  
Ken Yaga ◽  
Russel J. Reiter
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Cells ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Fetal Rat ◽  
Rat Pituitary ◽  
Lh Release ◽  
Rat Pituitary Cells

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.

SERUM LUTEINIZING HORMONE AND FOLLICLE-STIMULATING HORMONE CONCENTRATIONS IN IMMATURE FEMALE RATS TREATED WITH MULTIPLE INJECTIONS AND VARIOUS AMOUNTS OF LUTEINIZING HORMONE RELEASING HORMONE

1975 ◽  
Vol 66 (1) ◽  
pp. 13-20 ◽  
Author(s):  
D. C. JOHNSON ◽  
R. S. MALLAMPATI
Keyword(s):  
Luteinizing Hormone ◽  
Constant Stimulus ◽  
Female Rats ◽  
Intact Female ◽  
Immature Female ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Lh Rh

SUMMARY Release of immunoreactive LH and FSH was induced in immature intact female rats by repeated injections of synthetic luteinizing hormone releasing hormone (LH-RH). Altering the dose of LH-RH (5, 10, 20, 50 ng) and the frequency of administration (every 10, 20, 30 or 60 min) over a period of 2 h produced a variety of serum LH and FSH concentrations and ratios. When the dose was a constant 20 ng but the frequency of injections was either 20 or 30 min, a steady state in serum gonadotrophin concentrations was reached within 1 h and the level remained the same during the second hour. When given every 10 min, 20 ng LH-RH produced a much higher concentration of both LH and FSH during the second hour of stimulation. Examination of the gonadotrophin levels after each injection of LH-RH showed that the pituitary response was variable in spite of a constant stimulus.

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