Gonadotrophin-releasing hormone regulation of gonadotrophin subunit gene expression: studies in tri-iodothyronine-suppressed rats

1989 ◽  
Vol 122 (1) ◽  
pp. 117-125 ◽  
Author(s):  
D. J. Haisenleder ◽  
G. A. Ortolano ◽  
A. C. Dalkin ◽  
S. J. Paul ◽  
W. W. Chin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Blot Hybridization ◽  
Male Rats ◽  
Male Rat ◽  
Mrna Levels ◽  
Dot Blot ◽  
Α Subunit ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Prolactin Mrna

ABSTRACT We have previously shown that a pulsatile gonadotrophin-releasing hormone (GnRH) stimulus can increase steady-state levels of α and LH-β subunit mRNAs in the male rat pituitary. Since α subunit is produced in both thyrotroph and gonadotroph cells, the effect of GnRH specifically on gonadotroph α gene expression is uncertain. To address this tissue, adult male rats were given injections of tri-iodothyronine (T3; 20 μg/100 g body wt, i.p.) daily for 8 days (day 8 = day of death) in order to decrease thyrotroph α mRNA levels (+ T3 group). Saline injections (i.p.) were given to control animals (− T3 group). Three days before GnRH administration, the animals were castrated and testosterone implants inserted s.c., to inhibit endogenous GnRH secretion. GnRH pulses (25 ng/pulse; 30-min interval) were given to freely moving animals (saline pulses to controls) via an atrial cannula for 12, 24 or 48 h. Serum LH and FSH were measured before and 20 min after the last GnRH pulse. Pituitary RNA was extracted and α, LH-β, FSH-β and prolactin mRNA levels were determined by dot-blot hybridization using 32P-labelled cDNA probes. Castration and testosterone replacement reduced α and LH-β mRNA levels by 30 and 40% respectively, compared with levels in untreated intact males, but did not decrease FSH-β concentrations. T3 administration further decreased α mRNA to 30% of values seen in intact males, but LH-β mRNA levels were unchanged. FSH-β mRNA concentrations were decreased by 23% in T3-treated rats (P < 0·05 vs intact controls). In −T3 rats, 12 h of GnRH pulses increased FSH-β mRNA levels (twofold) vs saline-pulsed controls, but significant increases in α or LH-β mRNA levels were not seen until after 24 h of GnRH pulses. In the +T3 group, an increase in α mRNA was observed earlier, after 12 h of GnRH pulses. After 24 and 48 h of GnRH, the increments in α and LH-β were of similar magnitude in both the +T3 and − T3 groups (4–5 and 3–4 fold increases in α and LH-β respectively; P < 0·05 vs saline-pulsed controls). In contrast, the stimulatory effect of GnRH on FSH-β mRNA was lost in + T3 animals after 48 h of pulses. In order to examine whether this loss in FSH-β mRNA responsiveness to GnRH was related to an inhibitory interaction of T3 in the presence of testosterone, a second study was conducted in castrated animals. The results showed that α mRNA levels were decreased by 33% in +T3 compared with −T3 castrated animals (P < 0·05), but LH-β and FSH-β mRNAs were unaffected by T3 administration. In castrated animals given GnRH pulses, T3 inhibited subunit mRNA responses and this effect was most marked for FSH-β mRNA. In contrast, prolactin mRNA levels were significantly higher (P < 0·05) in all +T3 experimental groups compared with their −T3 controls. These data indicate that T3 can inhibit FSH-β mRNA responses to pulsatile GnRH and that this action occurs in the absence of testosterone. Journal of Endocrinology (1989) 122, 117–125

Gonadal regulation of pituitary hormone mRNA levels in male rats

1988 ◽  
Vol 1 (1) ◽  
pp. 61-68 ◽  
Author(s):  
S. D. Abbot ◽  
K. Docherty ◽  
R. N. Clayton
Keyword(s):  
Gene Expression ◽  
Male Rats ◽  
Male Rat ◽  
Pituitary Hormone ◽  
Mrna Levels ◽  
Subunit Gene ◽  
Α Subunit ◽  
Intact Control ◽  
Subunit Mrna ◽  
Serum Lh

ABSTRACT The control of anterior pituitary hormone gene expression by testosterone in male rat pituitaries in vivo was investigated using dot-blot mRNA-cDNA hybridization assays. Common α subunit mRNA levels doubled by 2 days after orchidectomy and rose progressively to reach plateau levels three to four times intact control values by 2 weeks. LH-β mRNA increased significantly (≃50%) within 12h, and thereafter progressively to seven times intact control values by 3 weeks after orchidectomy. The changes in α mRNA were likely to have occurred in gonadotrophs and not thyrotrophs, since TSH-β mRNA levels were unaltered by orchidectomy. LH subunit mRNA changes were accompanied by an initial (1–4 days) decrease in pituitary LH content; thereafter, pituitary LH increased in parallel with and by a similar magnitude to the LH-β mRNA. Serum LH rises occurred before significant increases in LH subunit mRNA after orchidectomy. The lack of temporal correlation between mRNA levels and serum and pituitary LH in the early stages after removal of testosterone feedback contrasts with the good correlation when a new steady state was achieved after 3–4 weeks, and indicates differing kinetics for changes in these aspects of gonadotroph function. An inhibitory effect of testosterone on LH subunit gene expression was confirmed by prevention of the rise in α and LH-β mRNAs when treatment commenced immediately after castration. However, pituitary LH content and serum LH levels were reduced relative to control values, suggesting additional inhibitory actions of testosterone on translational and post-translational events in gonadotrophs. A stimulatory effect of testosterone on α mRNA levels was observed between 4 and 24 h after a single injection in rats castrated 2 weeks previously, no effect being seen on LH-β mRNA. The mechanism for this action remains to be elucidated. Gene specificity of testosterone action was confirmed by unaltered levels of mRNA for prolactin, GH, TSH-β subunit and actin under all experimental conditions. No changes in pituitary content of prolactin or GH were found. We conclude that regulation of LH subunit gene expression by testosterone is an important step in control of gonadotrophin synthesis and availability for release.

Gonadotrophin-releasing hormone modulation of gonadotrophins in the ewe: evidence for differential effects on gene expression and hormone secretion

1991 ◽  
Vol 7 (1) ◽  
pp. 35-43 ◽  
Author(s):  
J. R. McNeilly ◽  
P. Brown ◽  
A. J. Clark ◽  
A. S. McNeilly
Keyword(s):  
Gene Expression ◽  
Gnrh Agonist ◽  
Hormone Secretion ◽  
Plasma Concentrations ◽  
Mrna Levels ◽  
Β Subunit ◽  
Subunit Gene ◽  
Α Subunit ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone

ABSTRACT While the regulation of gonadotrophin secretion by gonadotrophin-releasing hormone (GnRH) has been well documented in both rats and sheep, its role in the synthesis of gonadotrophin subunits remains unclear. We have investigated the effects of the specific inhibition of GnRH by a GnRH agonist on the expression of gonadotrophin subunit genes and the subsequent storage and release of both intact hormones and free α subunit. Treatment with GnRH agonist for 6 weeks abolished pulsatile LH secretion, reduced plasma concentrations of FSH and prevented GnRH-induced release of LH and FSH. This was associated with a reduction of pituitary LH-β mRNA and FSH-β mRNA levels (to 5 and 30% of luteal control values respectively), but not α mRNA which was significantly increased (75% above controls). While there was a small decrease in the pituitary content of FSH (30% of controls), there was a drastic reduction in LH pituitary content (3% of controls). In contrast to the observed rise in α mRNA, there was a decrease in free α subunit in both the pituitary and plasma (to 30 and 80% of control levels). These results suggest that, while GnRH positively regulates the expression of both gonadotrophin β-subunit genes, it can, under certain circumstances, negatively regulate α-subunit gene expression. Despite the complete absence of LH and FSH in response to GnRH, there remained a basal level of β-subunit gene expression and only a modest reduction (50%) in the plasma levels of both FSH and LH, suggesting that there is a basal secretory pathway. The dramatic reduction in LH pituitary content indicates that GnRH is required for the operation of a regulatory/storage pathway for the secretion of LH. There appears to be no similar mechanism for FSH. The LH-specific pathway is probably dependent upon the availability of LH-β subunits which subsequently plays a role in regulating α subunit by sequestering, assembling and storing the intact hormone in the presence of GnRH. Finally, in the absence of responsiveness to GnRH, the regulation of α-subunit production is not at the level of gene transcription. Inefficient translation of the mRNA or rapid degradation of the free α chain may account for the observed dramatic decrease in production of α subunit.

Relationship between gonadotrophin subunit gene expression, gonadotrophin-releasing hormone receptor content and pituitary and plasma gonadotrophin concentrations during the rebound release of FSH after treatment of ewes with bovine follicular fluid during the luteal phase of the cycle

1992 ◽  
Vol 8 (2) ◽  
pp. 109-118 ◽  
Author(s):  
J. Brooks ◽  
W. J. Crow ◽  
J. R. McNeilly ◽  
A. S. McNeilly
Keyword(s):  
Follicular Fluid ◽  
Luteal Phase ◽  
Gnrh Receptor ◽  
Mrna Levels ◽  
Α Subunit ◽  
Luteal Regression ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion ◽  
Cessation Of Treatment

ABSTRACT The modulation of FSH secretion at the beginning and middle of the follicular phase of the cycle represents the key event in the growth and selection of the preovulatory follicle. However, the mechanisms that operate within the pituitary gland to control the increased release of FSH and its subsequent inhibition in vivo remain unclear. Treatment of ewes with bovine follicular fluid (bFF) during the luteal phase has been previously shown to suppress the plasma concentrations of FSH and, following cessation of treatment on day 11, a rebound release of FSH occurs on days 12 and 13. When luteal regression is induced on day 12, this hypersecretion of FSH results in an increase in follicle growth and ovulation rate. To investigate the mechanisms involved in the control of FSH secretion, ewes were treated with twice daily s.c. injections of 5 ml bFF on days 3–11 of the oestrous cycle and luteal regression was induced on day 12 with prostaglandin (PG). The treated ewes and their controls were then killed on day 11 (luteal), or 16 or 32h after PG and their pituitaries removed and halved. One half was analysed for gonadotrophin and gonadotrophin-releasing hormone (GnRH) receptor content. Total pituitary RNA was extracted from the other half and subjected to Northern analysis using probes for FSH-β, LH-β and common α subunit. Frequent blood samples were taken and assayed for gonadotrophins. FSH secretion was significantly (P<0.01) reduced during bFF treatment throughout the luteal phase and then significantly (P<0.01) increased after cessation of treatment, with maximum secretion being reached 18– 22h after PG, and then declining towards control values by 32h after PG. A similar pattern of LH secretion was seen after bFF treatment. Pituitary FSH content was significantly (P<0.05) reduced by bFF treatment at all stages of the cycle. No difference in the pituitary LH content was seen. The increase in GnRH receptor content after PG in the controls was delayed in the treated animals. Analysis of pituitary mRNA levels revealed that bFF treatment significantly (P<0.01) reduced FSH-β mRNA levels in the luteal phase. Increased levels of FSH-β, LH-β and α subunit mRNA were seen 16h after PG in the bFF-treated animals, at the time when FSH and LH secretion from the pituitary was near maximum. These results suggest that the rebound release of FSH after treatment with bFF (as a source of inhibin) is related to a rapid increase in FSH-β mRNA, supporting the concept that the rate of FSH release is directly related to the rate of synthesis.

Effects of the gonadotrophin-releasing hormone agonist 'Zoladex' upon pituitary and gonadal function in hypogonadal (hpg) male mice: a comparison with normal male and testicular feminized (tfm) mice

1992 ◽  
Vol 8 (3) ◽  
pp. 249-258 ◽  
Author(s):  
I. S. Scott ◽  
M. K. Bennett ◽  
A. E. Porter-Goff ◽  
C. J. Harrison ◽  
B. S. Cox ◽  
...  
Keyword(s):  
Seminal Vesicle ◽  
Mrna Levels ◽  
Gonadal Function ◽  
Glycoprotein Hormone ◽  
Α Subunit ◽  
Releasing Hormone ◽  
Subunit Mrna ◽  
Serum Lh ◽  
Gonadotrophin Releasing Hormone ◽  
The Common

ABSTRACT Hypogonadal (hpg) mutant mice, with a congenital deficiency of hypothalamic gonadotrophin-releasing hormone (GnRH), and testicular feminized (tfm) mice, which lack a functional androgen receptor, were used to study the effects of the potent GnRH agonist 'Zoladex' (ICI 118630; d-Ser (But)6, Azgly10-GnRH) on pituitary and gonadal function. Zoladex (0.5 mg) in a sustained-release lactide—glycolide copolymer depot was administered subcutaneously under anaesthesia and was left in place for 7 days, after which time the effects of the drug upon pituitary and serum gonadotrophin concentrations, glycoprotein hormone subunit mRNAs and testicular morphology were investigated. At the pituitary level, Zoladex treatment resulted in a substantial reduction in LH content in normal males, and LH content was depressed in hpg mice even below the basal levels normally found in these mutants. Pituitary LH content in the Zoladex-treated animals was depressed in the tfm groups, but not to the same levels as those found in the normal and castrated normal mice. Zoladex treatment at the time of castration prevented the post-operative elevation in serum LH associated with castration alone. In the androgen-deficient tfm mouse, Zoladex did not depress the normally elevated serum LH levels. Serum LH in the hpg animals was, in all cases, below the limit of detection of the assay. Pituitary FSH content was depressed into the hpg range in both the normal and castrated animals, but there was no further depression in the hpg mice. The pituitary content was reduced in the tfm mice, again the effects not being as dramatic as in the normal and castrated animals. Serum FSH content, as measured by radioimmunoassay, was depressed by 50% in normal mice; there was no reduction in the hpg mice, however. With regard to pituitary gonadotrophic hormone gene expression, Zoladex administration to normal mice caused a dramatic reduction in LHβ mRNA content, to a level approximating that found in untreated hpg mice. The drug also depressed LHβ mRNA in the castrated group to the hpg range when given at the time of castration, whereas in untreated castrated mice there was a significant increase in LHβ mRNA. In the tfm mouse, which can be considered as a model for long-term failure of androgen feedback, Zoladex again induced a fall in LHβ mRNA, but not to the same extent as in the normal and normal castrated group. Zoladex had no effect on the already low levels of LHβ mRNA found in hpg mice. Pituitary FSHβ mRNA levels were not significantly altered by Zoladex in any of the treatment groups, whereas the drug induced a substantial rise in the common α-subunit mRNA in normal and hpg mice, to a level equalling that found in castrated tfm mice. In the latter two groups, Zoladex treatment did not result in a further increase in α-subunit mRNA above that found after castration alone, or in the untreated tfm mutant. Treatment for 7 days with Zoladex resulted in a significant increase in testis weight, with spermatogenesis advancing beyond the first meiotic division with many round spermatids found within the seminiferous tubules. However, the interstitial cells remained atrophic and there was evidence of seminal vesicle growth. Nevertheless, there was a small but significant increase in testicular androgen content. Administration of the agonist to hypophysectomized hpg mice did not stimulate testicular or seminal vesicle growth, suggesting that the drug does not stimulate steroidogenesis via a direct action upon the testis. Overall, the pharmacological effects of the drug appear to have turned off the transcription of the LHβ gene, with a consequent reduction in LH synthesis and probably also secretion in the longer term. With FSHβ, gene transcription was apparently unchanged and, with a substantial increase in the common α-subunit message, it would appear that the pituitary gland of Zoladex-treated animals may be predominantly biased towards FSH secretion. Although the circulating FSH levels as measured by radioimmunoassay were unaltered by Zoladex, there are several reports that GnRH agonists increase serum levels of bioactive hormones, perhaps by altering glycosylation of the FSH dimer glycoprotein.

Effect of short-term starvation on reproductive hormone gene expression, secretion and receptor levels in male rats

1989 ◽  
Vol 121 (3) ◽  
pp. 409-417 ◽  
Author(s):  
M. Bergendahl ◽  
A. Perheentupa ◽  
I. Huhtaniemi
Keyword(s):  
Male Rats ◽  
Ventral Prostate ◽  
Male Rat ◽  
Testicular Function ◽  
Mrna Levels ◽  
Short Term ◽  
Α Subunit ◽  
Gnrh Receptors ◽  
Androgen Synthesis ◽  
Serum Lh

ABSTRACT The effects of 4–6 days of food deprivation on the pituitary-testicular function of adult male rats were studied. Fasting decreased body weights on average by 23% (P<0·01) and those of seminal vesicles by 55% (P<0·01) in 4 days. No consistent changes were found in testicular and ventral prostate weights. The pituitary levels of gonadotrophin-releasing hormone (GnRH) receptors decreased by 50% (P<0·01). Serum and pituitary levels of LH, FSH and prolactin decreased by 25–50% (P<0·01 for all). Testicular and serum levels of testosterone decreased by 70–80%, testicular LH receptors by 26%, those of prolactin by 50% (P<0·01 for all), but those of FSH remained unaffected. Acute (2 h) stimulation by a GnRH agonist (buserelin, 10 μg/kg i.m.) resulted in similar LH, FSH and testosterone responses in the fasted and control animals, and human chorionic gonadotrophin (hCG) stimulation (30 IU/kg i.m.) in similar increases in testosterone. A 42% decrease was found in pituitary content of mRNA of the common α subunit (P<0·05), but the mRNAs of the LH- and FSH-β chains and prolactin were unaffected by fasting for 4 days. When the same mRNAs were measured after 6 days of fasting, the decrease of the mRNA of FSH-β also became significant (50%, P<0·01). In contrast, the mRNA of LH-β was increased twofold (P<0·01) at this time and serum LH levels were similar in control and starved animals. It is concluded that during short-term starvation of male rats: (1) the decrease in gonadotrophin and prolactin synthesis and secretion is first noticed on the level of translation (protein synthesis), and the mRNA levels of these hormones may respond more slowly to starvation, (2) decreased pituitary GnRH receptors indicate decreased GnRH release from the hypothalamus, (3)the gonadotrophin and prolactin loss results secondarily in decreased testicular androgen synthesis and LH and prolactin receptor levels, (4) no decrease occurs during starvation in acute gonadotrophin response to GnRH, or testicular testosterone response to hCG, (5) the primary response to starvation in male rat pituitary-testicular function is the loss of normal hypothalamic support of gonadotrophin and prolactin secretion, rather than direct nutritional effects on the pituitary and testis, and (6) when starvation is continued beyond 4 days, a recovery is seen in pituitary mRNA on the LH-β chain and in serum LH, most probably because the starvation-associated decrease serum testosterone is a more potent positive stimulus of LH synthesis than the direct hypothalamic-pituitary inhibition. Journal of Endocrinology (1989) 121, 409–417

scholarly journals LH down-regulates gonadotropin-releasing hormone (GnRH) receptor, but not GnRH, mRNA levels in the rat testis

1999 ◽  
Vol 162 (3) ◽  
pp. 409-415 ◽  
Author(s):  
MC Botte ◽  
Y Lerrant ◽  
A Lozach ◽  
A Berault ◽  
R Counis ◽  
...  
Keyword(s):  
Blot Hybridization ◽  
Fold Increase ◽  
Inhibitory Effect ◽  
Gonadotropin Releasing Hormone ◽  
Mrna Levels ◽  
Dot Blot ◽  
Releasing Hormone ◽  
Rat Testis ◽  
Gnrh Analogs ◽  
Serum Lh

The demonstration of an inhibitory effect of gonadotropin-releasing hormone (GnRH) agonists upon steroidogenesis in hypophysectomized rats and the presence of mRNA coding for GnRH and GnRH receptors (GnRH-R) in rat gonads suggests that GnRH can act locally in the gonads. To assess this hypothesis, we investigated the effects of GnRH analogs, gonadotropins and testosterone on the levels of both GnRH and GnRH-R mRNA in the rat testis. Using dot blot hybridization, we measured the mRNA levels 2 to 120 h after the administration of the GnRH agonist, triptorelin. We observed an acute reduction of both GnRH and GnRH-R mRNAs 24 h after the injection (about 38% of control). However, the kinetics for testis GnRH-R mRNA were different from those previously found for pituitary GnRH-R mRNA under the same conditions. Initially, the concentrations of serum LH and FSH peaked, then declined, probably due to the desensitization of the gonadotrope cells. In contrast, the GnRH antagonist, antarelix, after 8 h induced a 2.5-fold increase in GnRH-R mRNA, but not in GnRH mRNA, while gonadotropins levels were reduced. Human recombinant FSH had no significant effect on either GnRH or GnRH-R mRNA levels. Inversely, GnRH-R mRNA levels markedly decreased by 21% of that of control 24 h after hCG injection. Finally, 24 h after testosterone injection, a significant increase in GnRH-R mRNA levels (2.3 fold vs control) was found, but a reduction in the concentration of serum LH, probably by negative feedback on the pituitary, was observed. In contrast, GnRH mRNA levels were not significantly altered following testosterone treatment. Since LH receptors, GnRH-R and testosterone synthesis are colocalized in Leydig cells, our data suggest that LH could inhibit the GnRH-R gene expression or decrease the GnRH-R mRNA stability in the testis. However, this does not exclude the possibility that GnRH analogs could also affect the GnRH-R mRNA levels via direct binding to testicular GnRH-R. In contrast, the regulation of GnRH mRNA levels appeared to be independent of gonadotropins. Taken together, our results suggest a regulation of GnRH and GnRH-R mRNA specific for the testis.

Induction of the gonadotrophin surge-inhibiting factor by FSH and its elimination: a sex difference in the efficacy of the priming effect of gonadotrophin-releasing hormone on the rat pituitary gland

1993 ◽  
Vol 138 (2) ◽  
pp. 191-201
Author(s):  
D. W. Koppenaal ◽  
J. A. M. J. van Dieten ◽  
A. M. I. Tijssen ◽  
J. de Koning
Keyword(s):  
Body Weight ◽  
Pituitary Gland ◽  
Priming Effect ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Pulse Interval ◽  
Intact Female ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone

ABSTRACT This study was designed to explore the efficacy of gonadotrophin-releasing hormone (GnRH) to antagonize the effect of gonadotrophin surgeinhibiting factor (GnSIF) on the timing of the induction by GnRH of the maximal self-priming effect on pituitary LH responsiveness. The GnSIF levels were increased by FSH treatment and reduced after gonadectomy. Female rats were injected s.c. with 10 IU FSH or saline (control) on three occasions during the 4-day cycle. Serial i.v. injections of GnRH (500 pmol/kg body weight) were administered to intact rats on the afternoon of pro-oestrus or 15–30 min after ovariectomy. Intact male rats were given 10 IU FSH and 500 or 2000 pmol GnRH/kg body weight on an equivalent time-schedule. Endogenous GnRH release was suppressed with phenobarbital. In intact female control rats, the timing of the maximally primed LH response was delayed as the GnRH pulse-interval increased. FSH treatment of female rats induced a suppression of the initial unprimed LH response and delayed the maximally primed LH response, which showed further delay as the GnRH pulse-interval was increased. When the pulsatile administration of GnRH was started 15–30 min after ovariectomy, the priming effect of GnRH did not change as the GnRH pulse-interval was increased in the saline-treated rats. However, FSH treatment caused a suppression of the unprimed LH response, a delay in the primed LH response and decreased the delay of the maximally primed LH response to GnRH when the GnRH pulse-interval was decreased. Increasing the interval between ovariectomy and the first GnRH pulse to 4 h diminished the efficacy of the FSH treatment: GnRH-induced priming was delayed by only one pulse instead of the two pulses in control rats. In intact males but not in orchidectomized rats, a self-priming effect was demonstrated during GnRH pulses which were 1 h apart. The effect of 2 nmol GnRH/kg body weight was the most pronounced. Compared with intact female rats, the timing of the maximally primed LH response was delayed by 1 h. FSH treatment did not affect the pituitary LH response to both dose levels of GnRH. It is concluded that FSH treatment increased the release of GnSIF by the ovary, then induced a state of low responsiveness of the pituitary gland to GnRH and subsequently delayed GnRH-induced maximal self-priming. The efficacy of GnRH to prime the pituitary gland was higher when GnSIF levels were decreasing after removal of the ovaries. On the other hand, GnSIF was more effective when the GnRH pulse-interval was increasing. This allows GnSIF more time to restore the unprimed state of the pituitary gland after each GnRH pulse-induced self-priming effect. It remains a matter of debate whether a similar mechanism of action is present in the male rat or whether this mechanism is suppressed by endogenous hormones such as androgens. Journal of Endocrinology (1993) 138, 191–201

EFFECT OF ACTIVE IMMUNIZATION TO LUTEINIZING HORMONE RELEASING HORMONE ON SERUM AND PITUITARY GONADOTROPHINS, TESTES AND ACCESSORY SEX ORGANS IN THE MALE RAT

1974 ◽  
Vol 63 (2) ◽  
pp. 399-NP ◽  
Author(s):  
H. M. FRASER ◽  
A. GUNN ◽  
S. L. JEFFCOATE ◽  
DIANE T. HOLLAND
Keyword(s):  
Luteinizing Hormone ◽  
Active Immunization ◽  
Male Rats ◽  
Male Rat ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Accessory Sex Organs ◽  
Gonadotrophin Releasing Hormone ◽  
Low Levels ◽  
Lh Rh

SUMMARY Autoimmunity to luteinizing hormone releasing hormone (LH-RH) in adult male rats, induced by immunization with LH-RH conjugated to bovine serum albumin, resulted in atrophy of the testes and secondary sex organs and aspermatogenesis. Both immunoreactive luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in serum and the pituitary were reduced to low levels compared with those of control animals. It is suggested that antibodies to LH-RH can inhibit the action of endogenous hormone and that LH-RH is, in fact, the gonadotrophin-releasing hormone in the rat, required for the release of both LH and FSH.

scholarly journals Dynamics of Multiple lin Gene Expression in Sphingomonas paucimobilis B90A in Response to Different Hexachlorocyclohexane Isomers

2004 ◽  
Vol 70 (11) ◽  
pp. 6650-6656 ◽  
Author(s):  
Mrutyunjay Suar ◽  
Jan Roelof van der Meer ◽  
Kirsten Lawlor ◽  
Christof Holliger ◽  
Rup Lal
Keyword(s):  
Gene Expression ◽  
Sharp Increase ◽  
Blot Hybridization ◽  
Sphingomonas Paucimobilis ◽  
Mrna Levels ◽  
Dot Blot ◽  
Dot Blot Hybridization ◽  
Hch Isomers ◽  
Dynamic Expression ◽  
Hexachlorocyclohexane Isomers

ABSTRACT Sphingomonas paucimobilis B90A is able to degrade the α-, β-, γ-, and δ-isomers of hexachlorocyclohexane (HCH). It contains the genes linA, linB, linC, linD, linE, and linR, which have been implicated in HCH degradation. In this study, dynamic expression of the lin genes was measured in chemostat-grown S. paucimobilis B90A by RNA dot blot hybridization and real-time reverse transcriptase PCR upon exposure to a pulse of different HCH isomers. Irrespective of the addition of HCH, linA, linB, and linC were all expressed constitutively. In contrast, linD and linE were induced with α-HCH (2 mg/liter) and γ-HCH (7 mg/liter). A sharp increase in mRNA levels for linD and linE was observed from 10 to 45 min after the addition of α- or γ-HCH. Induction of linD and linE was not detectable upon the addition of 0.7 mg of γ-HCH per liter, although the compound was degraded by the cells. The addition of β-HCH (5 mg/liter) or δ-HCH (20 mg/liter) did not lead to linE and linD induction, despite the fact that 50% of the compounds were degraded. This suggests that degradation of β- and δ-HCH proceeds by a different pathway than that of α- and γ-HCH.

Changes in mRNA levels of a pituitary-specific trans-acting factor, Pit-1, and prolactin during the rat estrous cycle

1995 ◽  
Vol 132 (6) ◽  
pp. 771-776 ◽  
Author(s):  
Byung J Lee ◽  
Jin H Kim ◽  
Chae K Lee ◽  
Hae M Kang ◽  
Hyun C Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Estrous Cycle ◽  
Blot Hybridization ◽  
Mrna Level ◽  
Ovariectomized Rats ◽  
Mrna Levels ◽  
Cytoplasmic Rna ◽  
Slot Blot Hybridization ◽  
Prolactin Gene ◽  
Prolactin Mrna

Lee BJ, Kim JH, Lee CK, Kang HM, Kim HC, Kang SG. Changes in mRNA levels of a pituitary-specific trans-acting factor, Pit-1, and prolactin during the rat estrous cycle. Eur J Endocrinol 1995;132:771–6. ISSN 0804–4643 The present study examined the changes in mRNA levels of a pituitary-specific trans-acting factor, Pit-1, and prolactin during the rat estrous cycle. Total cytoplasmic RNA was analyzed by Northern blot and slot-blot hybridization to examine the prolactin mRNA level. Reverse transcription-polymerase chain reaction (RT-PCR) was performed to examine the Pit-1 mRNA level. Proestrous and estrous prolactin mRNA levels were significantly higher than the metestrous and diestrous levels, whereas Pit-1 mRNA levels of the estrous and metestrous stages were about two- to threefold higher than those of the proestrous and diestrous stages. Proestrous Pit-1 mRNA levels increased gradually from 10.00 h to 20.00 h, while prolactin mRNA levels slightly decreased until 14.00 h but increased later until 20.00 h. During the rat estrous cycle, especially in the afternoon of the proestrous day, changes of prolactin mRNA levels seem to follow a prior increase of Pit-1 mRNA. Therefore, Pit-1 may be partly involved in the regulation of prolactin gene expression according to the rat estrous cycle. Estradiol administration to ovariectomized rats significantly increased both the mRNA levels of prolactin and Pit-1, which suggests that the gene expression of Pit-1 is regulated by estrogen through indirect extracellular pathways. Byung Ju Lee, Department of Biology, College of Natural Sciences, University of Ulsan 680-749, Ulsan, South Korea

Sign in / Sign up

Export Citation Format

Share Document