Oxytocin-like signal regulates Lh cells directly but not Fsh cells in the ricefield eel Monopterus albus†

2020 ◽  
Author(s):  
Wei Yang ◽  
Ning Zhang ◽  
Yangsheng Wu ◽  
Lanxin Zhang ◽  
Lihong Zhang ◽  
...  
Keyword(s):  
Gonadal Development ◽  
Differential Regulation ◽  
Pituitary Cells ◽  
Female Fish ◽  
Monopterus Albus ◽  
Neuroendocrine Mechanisms ◽  
Lh Release ◽  
Lh Cells ◽  
Neuroendocrine Mechanism

Abstract The synthesis and release of LH and FSH in the pituitary of vertebrates are differentially regulated during gonadal development and maturation. However, the underlying neuroendocrine mechanisms remain to be fully elucidated. The present study examined the possible involvement of isotocin (Ist), an oxytocin-like neuropeptide, in the regulation of Lh and Fsh in a teleost, the ricefield eel Monopterus albus. The immunoreactive isotocin receptor 2 (Istr2) was shown to be localized to Lh but not Fsh cells. In contrast, immunoreactive isotocin receptor 1 (Istr1) was not observed in either Lh or Fsh cells in the pituitary. Interestingly, Lh cells in female ricefield eels expressed Istr2 and secreted Lh in response to Ist challenge stage-dependently and in correlation with ovarian vitellogenesis. Moreover, Ist decreased Lh contents in the pituitary of female fish, indicating its stimulatory roles on Lh release in vivo. The induction of Lh release by Ist in dispersed pituitary cells was blocked by a PLC or IP3R inhibitor but not by a PKA or PKC inhibitor, indicating the involvement of the IP3/Ca2+ pathway. Collectively, the above results indicate that isotocin may bind to Istr2 to stimulate Lh release via the IP3/Ca2+ pathway, and play important roles in the ovarian maturation in ricefield eels. Furthermore, the present study suggests a novel neuroendocrine mechanism underlying the differential regulation of Lh and Fsh in vertebrates.

scholarly journals Gnrh1-induced responses are indirect in female medaka Fsh cells

2019 ◽  
Author(s):  
Kjetil Hodne ◽  
Romain Fontaine ◽  
Eirill Ager-Wick ◽  
Finn-Arne Weltzien
Keyword(s):  
Patch Clamp ◽  
Adult Female ◽  
Reproductive Function ◽  
Cell Types ◽  
Gonadal Development ◽  
Pituitary Cells ◽  
Tissue Slices ◽  
Lh Cells ◽  
Different Cell Types

ABSTRACTReproductive function in vertebrates is stimulated by gonadotropin-releasing hormone (GnRH) that controls the synthesis and release of the two pituitary gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). FSH and LH, which regulates different stages of gonadal development, are produced by two different cell types in the fish pituitary, in contrast to mammals and birds, thus allowing the investigation of their differential regulation. In the present work, we show by fluorescentin situhybridization that Lh cells in adult female medaka express Gnrh receptors, whereas Fsh cells do not. This is confirmed by patch clamp recordings and cytosolic Ca2+measurements on dispersed pituitary cells, where Lh cells, but not Fsh cells, respond to Gnrh1 by increased action potential frequencies and cytosolic Ca2+levels. In contrast, both Fsh and Lh cells are able to respond electrically and by elevating the cytosolic Ca2+levels to Gnrh1 in brain-pituitary tissue slices. Using Ca2+uncaging in combination with patch clamp recordings and cytosolic Ca2+measurements, we show that Fsh and Lh cells form homo- and heterotypic networks in the pituitary. Taken together, these results show that the effects of Gnrh1 on Fsh release in adult female medaka is indirect, likely mediated via Lh cells.

Stimulatory effect of thyrotrophin-releasing hormone (TRH) on the release of luteinizing hormone (LH) from rat anterior pituitary cells in vitro

1983 ◽  
Vol 61 (2) ◽  
pp. 186-189 ◽  
Author(s):  
Noboru Fujihara ◽  
Masataka Shiino
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Anterior Pituitary Cells ◽  
Lh Release ◽  
Lh Rh

The effect of thyrotrophin-releasing hormone (TRH, 10−7 M) on luteinizing hormone (LH) release from rat anterior pituitary cells was examined using organ and primary cell culture. The addition of TRH to the culture medium resulted in a slightly enhanced release of LH from the cultured pituitary tissues. However, the amount of LH release stimulated by TRH was not greater than that produced by luteinizing hormone – releasing hormone (LH–RH, 10−7 M). Actinomycin D (2 × 10−5 M) and cycloheximide (10−4 M) had an inhibitory effect on the action of TRH on LH release. The inability of TRH to elicit gonadotrophin release from the anterior pituitary glands in vivo may partly be due to physiological inhibition of its action by other hypothalamic factor(s).

Effects of lithium and phorbol on the dynamics of LH release from dispersed sheep pituitary cells

1986 ◽  
Vol 111 (1) ◽  
pp. 167-173 ◽  
Author(s):  
L. Starling ◽  
R. P. McIntosh ◽  
E. A. Mclntosh
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Inositol Phosphates ◽  
Pituitary Cells ◽  
Kinase C ◽  
Dependent Protein ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Cells ◽  
Activate Protein Kinase

ABSTRACT The possible involvement of polyphosphoinositides in the stimulation of LH release was investigated. Dispersed sheep pituitary cells were incubated in test-tubes, or perifusedns in columns, with gonadotrophin-releasing hormone (GnRH) and Li+, or with a phorbol ester, and the amounts and patterns of LH release over time compared. Treatment with Li+ (10 mmol/l), which is known to increase levels of inositol phosphates in gonadotrophs, was shown to have effects only on the responses of desensitized cells, significantly decreasing the rate at which the cells desensitize (P<0·005) and decreasing the response to supramaximal levels of GnRH stimulus (P<0·01). It is suggested that these effects could be due to increased levels of inositol monophosphate, inositol bisphosphate inositol 1,3,4-trisphosphate. Responses to single or repeated pulses of GnRH at 18-, 30- and 60-min intervals were not significantly altered. Phorbol 12-myristate 13-acetate (PMA), an activator of the calcium and phospholipid-dependent protein kinase (protein kinase C), was specifically active in releasing LH with a half-maximal stimulating dose of approximately 3 nmol/l. Phorbol 12,13-diacetate, which is structurally similar to PMA but does not activate protein kinase C, did not release LH, except at high levels in freshly dispersed cells. The timing of PMA-stimulated LH release was similar to that for GnRH-stimulated release, and PMA was able to release greater amounts of LH than could GnRH. This suggests that activation of protein kinase C is likely to be important in the GnRH-stimulated release of LH from gonadotrophs. It also shows that the desensitization to GnRH stimulation observed after 10 min is unlikely to be caused by lack of releasable LH. Cells desensitized to maximally stimulating levels of GnRH still responded strongly to PMA stimulation, indicating that the desensitization to GnRH stimulation involves a step in the transduction mechanism before activation of protein kinase C. J. Endocr. (1986) 111, 167–173

Oxytocin stimulates LH production by the anterior pituitary gland of the rat

1992 ◽  
Vol 132 (2) ◽  
pp. 277-283 ◽  
Author(s):  
G. Robinson ◽  
J. J. Evans ◽  
K. J. Catt
Keyword(s):  
Female Rats ◽  
Release Mechanism ◽  
Protein Synthesis Inhibitor ◽  
Pituitary Cells ◽  
Synthesis Inhibitor ◽  
Mechanical Dispersion ◽  
Lh Release

ABSTRACT Gonadotrophin-releasing activity of oxytocin has previously been demonstrated in vitro and in vivo. This study investigated whether oxytocin is also able to induce LH accumulation in pituitary cells. Following trypsin digestion and mechanical dispersion, pituitary cells from female rats were incubated with oxytocin (100 nmol/l) for 24 h. LH release stimulated by oxytocin increased (P < 0·001) progressively during the incubation indicating a different secretory pattern from the more rapid but less sustained secretion stimulated by gonadotrophin-releasing hormone. Oxytocin also enhanced (P < 0·01) total LH accumulation in the incubation system (released plus cell contents) which was apparent after 7–11 h of stimulation. The release of LH stimulated by oxytocin was reduced by the protein synthesis inhibitor cycloheximide (10 μmol/l). However, cycloheximide did not completely block oxytocin-stimulated LH release; there remained some LH release above that seen in non-stimulated controls (P < 0·01) revealing the presence of a cycloheximide-resistant component in the release mechanism. Furthermore, accumulation of total LH in 24 h incubations was suppressed (P < 0·01) by cycloheximide. The advancement in LH release which oxytocin has been shown to induce in vivo in pro-oestrous rats was accompanied by an early reduction of pituitary LH stores. However, the fall normally observed in LH content during the surge was markedly attenuated by the oxytocin treatment. Thus, loss of pituitary LH stores was less in oxytocin-treated rats than in saline-treated controls, even though net LH release into plasma was increased. Therefore, oxytocin stimulated the replenishment of LH stores. Although the mechanism(s) remains to be defined and the relationships between in-vitro and in-vivo results are as yet uncharacterized, the present study demonstrates that oxytocin treatment stimulates LH production in both dispersed cells and intact pituitaries in situ. Journal of Endocrinology (1992) 132, 277–283

Effects of crude and highly purified bovine inhibin (Mr 32 000 form) on gonadotrophin production by ovine pituitary cells in vitro: inhibin enhances gonadotrophin-releasing hormone-induced release of LH

1990 ◽  
Vol 127 (1) ◽  
pp. 149-159 ◽  
Author(s):  
S. Muttukrishna ◽  
P. G. Knight
Keyword(s):  
Primary Cultures ◽  
Suppressive Effect ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Α Subunit ◽  
Releasing Hormone ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone

ABSTRACT Primary cultures of ovine pituitary cells (from adult ewes) were used to investigate the actions of steroid-free bovine follicular fluid (bFF) and highly-purified Mr 32 000 bovine inhibin on basal and gonadotrophin-releasing hormone (GnRH)-induced release of FSH and LH. Residual cellular contents of each hormone were also determined allowing total gonadotrophin content/well to be calculated. As in rats, both crude and highly purified inhibin preparations promoted a dose (P < 0·001)- and time (P < 0·001)-dependent suppression of basal and GnRH-induced release of FSH as well as an inhibition of FSH synthesis, reflected by a fall in total FSH content/well. However, while neither inhibin preparation affected basal release of LH or total LH content/well, GnRH-induced LH release was significantly (P< 0·001) increased by the presence of either bFF (+ 75%) or highly-purified inhibin (+ 64%) in a dose- and time-dependent manner. This unexpected action of bFF on GnRH-induced LH release was abolished in the presence of 5 μl specific anti-inhibin serum, confirming that the response was indeed mediated by inhibin. Furthermore, neither oestradiol-17β (1 pmol/l–10 nmol/l) nor monomeric α-subunit of bovine inhibin (2·5–40 ng/ml) significantly affected basal or GnRH-induced release of LH. These in-vitro findings for the ewe lend support to a number of recent in-vivo observations and indicate that, in addition to its well-documented suppressive effect on the synthesis and secretion of FSH, inhibin may actually facilitate LH release in this species, in marked contrast to its action in the rat. Journal of Endocrinology (1990) 127, 149–159

The effect of gonadotrophin surge-inhibiting factor on the self-priming action of gonadotrophin-releasing hormone in female rats in vitro

1992 ◽  
Vol 134 (3) ◽  
pp. 427-436 ◽  
Author(s):  
D. W. Koppenaal ◽  
A. M. I. Tijssen ◽  
J. de Koning
Keyword(s):  
Protein Synthesis ◽  
Priming Effect ◽  
The Self ◽  
Pituitary Cells ◽  
Inhibiting Factor ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Functional Antagonism

ABSTRACT The present study was designed to explore further the functional antagonism between gonadotrophin-releasing hormone (GnRH) and the ovarian factor, gonadotrophin surge-inhibiting factor (GnSIF). In all experiments, pituitary tissue was exposed to various amounts of GnSIF, after which the self-priming action of GnRH was studied. GnSIF was increased in vivo by FSH treatment and increased in vitro by adding various amounts of follicular fluid (FF) to cultured pituitary cells. Treatment with 3 or 10 IU FSH suppressed the initial LH response and delayed the maximally primed LH response to GnRH. Treatment with FSH was only effective in intact rats on days 1 and 2 of dioestrus. There was no difference in the rate of maximal LH release irrespective of treatment with either FSH or saline. Since FSH treatment was ineffective in long-term ovariectomized rats, it was concluded that the initial suppressive effect of FSH on LH release was mediated by GnSIF. Cycloheximide prevented the self-priming action of GnRH by inhibiting GnRH-induced protein synthesis. The initial protein synthesis-independent GnRH-stimulated LH release, which was already suppressed by FSH treatment, remained suppressed in the presence of cycloheximide. Pretreatment with GnRH in vivo increased the protein synthesis-independent GnRH-induced LH release during subsequent incubation of the glands. This increase did not occur after FSH treatment. Pituitary cells, cultured for 20 h in medium only, failed to elicit the self-priming effect of GnRH. Preincubation with FF maintained the self-priming effect. This was independent of the concomitant presence of various amounts of oestradiol. Preincubation with bovine FF suppressed the initial GnRH-stimulated LH release dose-dependently. Porcine FF, human FF and testicular extract suppressed the release of LH in a similar way. It was concluded that GnSIF suppresses the initial LH response to continuous GnRH stimulation. Increased levels of GnSIF caused by FSH treatment also delayed the primed LH release. The mechanism of functional antagonism between GnSIF and GnRH could give rise to the occurrence of the phenomenon of GnRH self-priming. Journal of Endocrinology (1992) 134, 427–436

Oxytocin has a role in gonadotrophin regulation in rats

1990 ◽  
Vol 125 (3) ◽  
pp. 425-432 ◽  
Author(s):  
G. Robinson ◽  
J. J. Evans
Keyword(s):  
Follicular Development ◽  
Pituitary Cells ◽  
Lh Surge ◽  
Rat Pituitary ◽  
Lh Release ◽  
Rat Pituitary Cells ◽  
Dose Dependent ◽  
In Vivo Administration

ABSTRACT We previously demonstrated that oxytocin stimulates LH release from rat pituitary cells in vitro and advances follicular development and ovulation in mice in vivo. This study reports an investigation of rat LH levels following in-vivo administration of oxytocin. Injection of oxytocin (10 mIU/g, i.p.) to rats at 07.00, 08.00 and 09.00 h of pro-oestrus or at 09.00, 10.00 and 11.00 h of pro-oestrus advanced the onset of the LH surge (P<0.005) and attainment of peak concentrations of LH (P<0.02) in peripheral blood. On the other hand, the descending phase of the LH surge and the surge amplitude were not altered by oxytocin. Treatment at 05.00, 06.00 and 07.00 h of pro-oestrus or at 11.00, 12.00 and 13.00 h of pro-oestrus had no effect on the LH profile. A higher oxytocin dose (20 mIU/g) inhibited LH release when treatment was begun at 05.00, 07.00 or 09.00 h of pro-oestrus. A lower dose (5 mIU/g) was ineffective in altering LH concentrations. In addition, injections of oxytocin (10 mIU/g) at oestrus, metoestrus or dioestrus had no effect on the release of LH. Thus the efficacy of oxytocin in altering concentrations of LH was dose dependent and also critically affected by the day of the oestrous cycle and the time of pro-oestrus. Removal of endogenous oxytocin activity by the use of an oxytocin receptor antagonist abolished the pro-oestrous LH surge, indicating that oxytocin is a vital physiological component of the LH-releasing mechanism in rats. The study provides unequivocal evidence that oxytocin induces LH release in vivo, but the manifestation of oxytocin activity is dependent upon conditions of exposure. Journal of Endocrinology (1990) 125, 425–432

scholarly journals Acceleration of maturation of FSH and LH responses to photostimulation in prepubertal domestic hens by oestrogen

Reproduction ◽  
2003 ◽  
pp. 217-225 ◽  
Author(s):  
IC Dunn ◽  
PD Lewis ◽  
PW Wilson ◽  
PJ Sharp
Keyword(s):  
Egg Laying ◽  
Paracrine Factors ◽  
Oestrogen Treatment ◽  
Oestradiol Benzoate ◽  
Before And After ◽  
Neuroendocrine Mechanisms ◽  
Lh Release ◽  
Neuroendocrine Mechanism

Egg laying begins in domestic hens, reared on short daylengths, at about day 147 of age and is advanced by photostimulation after but not before about day 42 of age. The development of this response at day 42 may be facilitated by oestrogen. This hypothesis was investigated in prepubertal hens, reared on short daylengths, by comparing the effects of oestrogen treatment on pituitary and plasma FSH and LH responses to photostimulation (16 h light:8 h dark) for 1 week at days 34 and 54 of age. Oestradiol benzoate (0.5 mg kg(-1)) was injected i.m. on alternate days for 1 week before and after photostimulation. At day 34, pituitary LH content increased after photostimulation but plasma LH and FSH concentrations did not increase. At day 54, pituitary FSH content and plasma FSH and LH concentrations increased after photostimulation, whereas pituitary LH content did not increase. At days 34 and 54, oestrogen treatment decreased pituitary FSH and LH contents but did not block the stimulatory effect of photostimulation on pituitary FSH. At day 34 but not at day 54, photostimulation combined with oestrogen treatment increased plasma FSH and LH concentrations. Plasma LH but not plasma FSH concentration increased after GnRH-I injection at days 34 and 54. These observations are consistent with the hypothesis that, in prepubertal female chickens, maturation of the neuroendocrine mechanism mediating photoinduced FSH and LH release may be mediated by oestrogen. This effect of oestrogen on photoinduced LH release may be mediated by increased GnRH-I release or enhanced pituitary responsiveness to GnRH-I. It is proposed that neuroendocrine mechanisms controlling photoinduced FSH release may involve oestrogen-responsive interactions between pituitary paracrine factors, including activins and follistatin.

scholarly journals The Presence and Ancestral Role of Gonadotropin-Releasing Hormone in the Reproduction of Scleractinian Coral, Euphyllia ancora

Endocrinology ◽  
2006 ◽  
Vol 147 (1) ◽  
pp. 397-406 ◽  
Author(s):  
Wen-Hung Twan ◽  
Jiang-Shiou Hwang ◽  
Yan-Horn Lee ◽  
Shan-Ru Jeng ◽  
Wen-Shiun Yueh ◽  
...  
Keyword(s):  
Biological Activity ◽  
Scleractinian Coral ◽  
Fold Increase ◽  
Aromatase Activity ◽  
Pituitary Cells ◽  
Oocyte Growth ◽  
Spawning Period ◽  
In Vivo Experiments ◽  
Lh Release

The objectives of this study were to investigate the presence of immunoreactive GnRH (irGnRH) in scleractinian coral, Euphyllia ancora, study its seasonal variation, and evaluate its biological activity. irGnRH was detected and quantified in coral polyps. The biological activity of coral irGnRH was tested on pituitary cells from black porgy by evaluating its ability to stimulate LH release. Coral extracts (10−9–10−5m irGnRH) as well as mammalian (m) GnRH agonist (10−10–10−6m) had a similar dose-dependent effect on LH release. Furthermore, GnRH receptor antagonist dose-dependently inhibited the stimulation of LH release in response to coral extracts (10−5m irGnRH) and mGnRH agonist (10−6m). Peak levels of irGnRH (10-fold increase) were observed during the spawning period in a 3-yr investigation. Significantly higher aromatase activity and estradiol (E2) levels were also detected during the period of spawning compared with the nonreproductive season. In in vivo experiments, mGnRH agonist time- and dose-dependently stimulated aromatase activity as well as the concentrations of testosterone and E2 in free and glucuronided forms in coral. In conclusion, our data indicate that irGnRH does exist in coral, with its ability to stimulate LH release in fish. Seasonal variations of coral irGnRH, with a dramatic increase during the spawning period, concomitant to that in aromatase and E2, as well as the ability of mGnRH agonist to stimulate coral aromatase, steroidogenesis, and steroid glucuronization suggest that irGnRH plays an important role in the control of oocyte growth and mass spawning in corals.

Effect of chronic exposure to a gonadotrophin-releasing hormone agonist on in vitro responsiveness of ovine pituitary cells to inhibin, activin and oestradiol

1994 ◽  
Vol 140 (3) ◽  
pp. 483-493 ◽  
Author(s):  
S Muttukrishna ◽  
P G Knight
Keyword(s):  
Gnrh Agonist ◽  
Inhibitory Effect ◽  
Pituitary Cells ◽  
Cell Content ◽  
Releasing Hormone ◽  
Basal Release ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone

Abstract To investigate the extent to which the direct actions of inhibin, activin and oestradiol on pituitary output of FSH and LH are dependent on the presence of functional gonadotrophin-releasing hormone (GnRH) receptors, we have compared the effects of these agents on cultured ovine pituitary cells derived from control and GnRH agonist-suppressed ewes. Chronic treatment with GnRH agonist reduced plasma LH and FSH levels (P<0·01) and abolished GnRH-induced release of LH and FSH both in vivo and in vitro. As expected, basal LH release and LH cell content in vitro were drastically reduced in GnRH agonist-suppressed cells (P<0·001). However, basal FSH release and FSH cell content were approximately twofold higher than in control cells (P<0·001). Irrespective of whether the cells had been desensitized to GnRH, inhibin and oestradiol were both found to suppress basal FSH release and FSH cell content in a dose-dependent fashion (P<0·001). Although inhibin had no effect on basal release of LH from control cells, it markedly enhanced GnRH-induced release (P<0·001). In contrast, inhibin increased (P<0·001) basal LH release from GnRH agonist-suppressed cells (which were unresponsive to the GnRH challenge). Inhibin had no overall effect on total LH content/well for either control or GnRH agonist-suppressed cells. Treatment with oestradiol, on the other hand, reduced total LH content/well, an effect which was more pronounced with GnRH agonist-suppressed cells (−44%; P<0·001) than with control cells (−14%, P<0·01). Whereas in control cells activin had no significant effect on any aspect of FSH production examined, in GnRH agonist-treated cells activin enhanced basal FSH release, residual cell content and total FSH content/well (P<0·001). Altering GnRH receptor status also modified the LH response to activin. With control cells activin increased basal release (P<0·001), decreased GnRH-induced release (P<0·001) and increased total LH content/well (P<0·001). With GnRH agonist-treated cells, however, activin had a uniform inhibitory effect on each aspect of LH production examined (P<0·001 in each case). It was concluded that desensitization of ovine gonadotrophs to GnRH by chronic agonist treatment results in a paradoxical enhancement of FSH output in vitro but has little effect on the responsiveness of the cells (in terms of gonadotrophin release and content) to either inhibin or oestradiol. In contrast, GnRH agonist treatment leads to qualitative changes in cellular reponsiveness to activin. Journal of Endocrinology (1994) 140, 483–493

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