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

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.

1975 ◽  
Vol 64 (1) ◽  
pp. 27-35 ◽  
Author(s):  
F. R. BURNET ◽  
P. C. B. MACKINNON

SUMMARY The rate of [35S]methionine incorporation into protein in discrete cerebral areas was measured before and after the administration of oestradiol benzoate (OB) to chronically ovariectomized rats. The circadian rhythm of incorporation which is normally seen in the intact cyclic female rat was deleted by ovariectomy. A daily rhythm of incorporation reappeared, however, in all the brain areas studied 30 h after a single injection of OB (20 μg), and was still present 12 days later. The release of luteinizing hormone (LH) after administration of 20 μg OB was measured in chronically ovariectomized animals and was found to be biphasic. High levels of LH after ovariectomy were initially reduced by negative feedback, but this phase was followed 52 h later by a facilitation of LH release between 15.00 and 18.00 h. The facilitation of LH release at this time of day was still detectable 12 days after the initial injection. The evidence for a functional link between the rhythm of neural activity which is reflected by [35S]methionine incorporation, and the ability to 'time' the facilitation of LH release is discussed.


1993 ◽  
Vol 139 (2) ◽  
pp. 253-258 ◽  
Author(s):  
A. M. Salicioni ◽  
R. W. Carón ◽  
R. P. Deis

ABSTRACT There is evidence that the adrenals play a role in the regulation of the synthesis and release of gonadotrophins in various vertebrates. The aim of this study was to determine the part played by adrenal steroids, with special reference to progesterone, on the concentration of LH in ovariectomized (OVX) and oestrogen-primed rats. OVX rats received a single s.c. injection of vehicle or oestradiol benzoate (OB, 20 μg/rat). This day was designated as day 0. Three or four days later (day 3–day 4), the rats were treated with mifepristone (10 mg/kg) or with two doses of progesterone antiserum and blood samples were obtained at 13.00 and 18.00 h. OB treatment of OVX rats reduced serum LH at 13.00 h and 18.00 h on day 3 but only at 13.00 h on day 4. The administration of mifepristone at 08.00 h to OVX and oestrogen-treated rats induced a significant increase in serum LH at 18.00 h on days 3 and 4, without modifying the values at 13.00 h. When mifepristone was given at 13.00 h a much larger increase in serum LH was obtained at 18.00 h. In OVX and oestrogen-treated rats, adrenalectomy on day 2 (08.00–09.00 h) induced an increase in serum LH at 18.00 h similar to that observed in the OVX and oestrogen-primed rats after mifepristone treatment. In order to determine the specificity of the effect of mifepristone, a group of OVX and oestrogentreated rats was injected with progesterone antiserum at 08.00 and 13.00 h on day 3. Serum LH concentrations at 13.00 and 18.00 h on day 3 were similar to values obtained in OVX rats treated with oestrogen and mifepristone. Serum progesterone was measured at 08.00 and 13.00 h in OVX and OVX and oestrogenprimed rats. At both times, values were similar in OVX rats but oestrogen treatment significantly increased serum progesterone levels. The important role of adrenal progesterone on the regulation of LH secretion in OVX and oestrogen-primed rats is evident from these results. Blocking progesterone action at the receptor level, we showed that OB significantly increased LH values at 18.00 h. On the basis of these studies it is tempting to speculate on the possibility of an inhibitory or stimulatory effect of oestrogen on serum LH concentration in OVX rats, according to the presence or absence of adrenal progesterone action. Journal of Endocrinology (1993) 139, 253–258


Author(s):  
Wei Yang ◽  
Ning Zhang ◽  
Yangsheng Wu ◽  
Lanxin Zhang ◽  
Lihong Zhang ◽  
...  

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.


1982 ◽  
Vol 94 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Takashi Higuchi ◽  
Masazumi Kawakami

Changes in the characteristics of LH secretory pulses in female rats were determined in different hormonal conditions; during the oestrous cycle and after ovariectomy and oestrogen treatment. The frequency and amplitude of the LH pulses were stable during the oestrous cycle except at oestrus when a pattern could not be discerned because of low LH concentrations. These were significantly lower than those measured during other stages of the cycle. Mean LH concentrations and LH pulse amplitudes increased with time up to 30 days after ovariectomy. The frequency of the LH pulse was unchanged 4 days after ovariectomy when mean LH levels had already increased. The frequency increased 10 days after ovariectomy and then remained stable in spite of a further increase in mean serum LH concentrations. Oestradiol-17β injected into ovariectomized rats caused a decrease in LH pulse amplitude but no change in pulse frequency. One day after treatment with oestradiol benzoate no LH pulse was detectable, probably because the amplitude was too small. A generator of pulsatile LH release is postulated and an oestrogen effect on its function is discussed.


1982 ◽  
Vol 92 (3) ◽  
pp. 327-339 ◽  
Author(s):  
E. TERASAWA ◽  
J. NOONAN ◽  
W. E. BRIDSON

Although the anterior pituitary gland has been shown to be a site of oestrogen feedback in the non-human primate, the role of the hypothalamus as a site of ovarian steroid feedback in facilitating gonadotrophin release has not been ruled out. In the present study, LH release in response to 2·5 mg progesterone with oestradiol benzoate (OB; 10 μg or 30 μg) 30 h earlier was observed in the ovariectomized monkey. Then pentobarbitone sodium was administered to block the progesterone-induced LH response. Serum levels of LH, oestradiol (OE2) and progesterone were measured by radioimmunoassay. In the first series of experiments a group of nine rhesus monkeys received subcutaneous implants of a small silicone elastomer capsule containing OE2. Two weeks later, either OB and oil, or OB and progesterone were injected sequentially. Oestradiol benzoate (10 μg) followed by oil 30 h later failed to cause any clear LH release, while 30 μg OB followed by oil induced a single peak of LH release with a peak latency of 16·5 ± 1·9 (s.e.m.) h after oil, and a duration of 69·8 ± 10·2 h. Regardless of the dose of OB, however, progesterone induced an LH release with two peaks in all animals. The peak latency (7·3 ±0·9 h) and the duration (19·3 ±1·3 h) of the first response with 30 μg OB + progesterone were virtually identical to those with 10 μg OB + progesterone (7·0 ±0·7 h, 18·0 ± 1·4 h respectively), whilst both components of the first response with 30 μg OB + progesterone were significantly shorter than those with 30 μg OB + oil (P < 0·001 for both). The peak latency of the second response with 30 μg OB + progesterone (42·7+ 4·8 h) was similar to that with 10 μg OB + progesterone (38·3 ±3·2 h), but the duration of the second response with 30 μg OB + progesterone (46·0 ± 1·7 h) was longer than that (35·7 ±3·2 h) with 10 μg OB + progesterone (P <0·02). In the second series of experiments the same nine animals received an OE2-capsule implantation and 10 μg OB (subthreshold) injections before pentobarbitone and progesterone. Pentobarbitone was first given 6 h before progesterone and additional injections were made to maintain the anaesthetized state for 21·6 ± 1·3 h. This period was to cover the progesterone-induced first LH response. Pentobarbitone completely blocked the expected first response of the progesterone-induced LH release in six animals. In the remaining three animals an enhanced LH surge occurred, but it consisted of a single peak with long latency 16·0 ± 2·0 h) and duration (66·0 ± 10·5 h) and was essentially the same as that observed in animals treated with a suprathreshold dose (30 μg) of OB alone. Anaesthesia did not, on the other hand, alter the response of the pituitary gland to LH releasing hormone. Therefore it was concluded that (1) sequential administration of oestrogen and progesterone induces an LH release with two phases in the ovariectomized monkey and (2) the facilitatory action of progesterone on the first phase of LH release requires the involvement of the brain.


2016 ◽  
Vol 60 (2) ◽  
pp. 119-128
Author(s):  
Georgios Goras ◽  
Chrysoula Tananaki ◽  
Sofia Gounari ◽  
Elissavet Lazaridou ◽  
Dimitrios Kanelis ◽  
...  

Abstract We investigated the rearing of drone larvae grafted in queen cells. From the 1200 drone larvae that were grafted during spring and autumn, 875 were accepted (72.9%) and reared as queens. Drone larvae in false queen cells received royal jelly of the same composition and of the same amounts as queen larvae. Workers capped the queen cells as if they were drones, 9-10 days after the egg laying. Out of 60 accepted false queen cells, 21 (35%) were capped. The shape of false queen cells with drone larvae is unusually long with a characteristically elongate tip which is probably due to the falling of larvae. Bees start the destruction of the cells when the larvae were 3 days old and maximised it before and after capping. Protecting false queen cells in the colony by wrapping, reversing them upside down, or placing in a horizontal position, did not help. The only adult drones that emerged from the false queen cells were those protected in an incubator and in push-in cages. Adult drones from false queen cells had smaller wings, legs, and proboscis than regular drones. The results of this study verify previous reports that the bees do not recognise the different sex of the larvae at least at the early stage of larval development. The late destruction of false queen cells, the similarity in quality and quantity of the produced royal jelly, and the bigger drone cells, allow for the use of drone larvae in cups for the production of royal jelly.


1959 ◽  
Vol 18 (1) ◽  
pp. 108-117 ◽  
Author(s):  
R. W. NOYES ◽  
C. E. ADAMS ◽  
A. WALTON

SUMMARY In order to determine what part the level of oestrogen in the body might play in the passage of ova through the female reproductive tract, 1249 freshly ovulated ova from donor rabbits were transferred into the uterine tubes of seventy-four ovariectomized recipients, fifty-three of which had previously been treated for 5–18 days with small daily injections of oestradiol benzoate. From 10 to 78 hr after transfer, 41% of the ova were recovered from the uterine tubes, 9% from the uterine horns, and 23% from the vaginae of the recipient animals. Twenty-seven% of the ova were lost. The rate of ovum transport varied widely between similarly treated animals, and between the right and left sides of the reproductive tract of the same animal. Larger proportions of ova were retained in the uterine tubes, and smaller proportions in the uterine horns as the oestrogen dose was increased. The great variability in the stage of cleavage and in the thickness of the mucin coat of ova recovered from the uterus and vagina suggested that the ova might be widely dispersed through the uterine tubes and that they probably pass out of the uterine tube at widely different periods of time. Evidence is presented that ovum transport in ovariectomized rabbits with or without oestrogen treatment is very irregular, that ova may be ejected from either end of the uterine tube at almost any time after transfer, and that ova are not normally retained in the uteri of such animals. Approx. 1 μg oestradiol benzoate administered daily for 5–10 days was necessary to maintain the uterine weight of ovariectomized rabbits at about the same level as that in intact oestrous rabbits, and also to reduce the variability in egg transport observed in control and ovariectomized animals.


1985 ◽  
Vol 106 (1) ◽  
pp. 37-42 ◽  
Author(s):  
C. Hiemke ◽  
B. Poetz ◽  
R. Ghraf

ABSTRACT Long-term (4–6 weeks) ovariectomized rats were injected with either oestradiol benzoate (OB; 20 μg s.c.) or monohydroxytamoxifen (MTAM; 0·2 mg i.p.) plus OB. Oestradiol benzoate was administered at 12.00 h on day 0 and MTAM was given immediately before OB, followed by further injections twice daily to maintain sufficiently high antioestrogen levels. When given alone, OB reduced the serum levels of LH during the morning (08.00–09.00 h) and afternoon (17.30–18.30 h) hours of day 3 after priming. The feedback actions of OB on LH release were accompanied by time-dependent alterations of noradrenaline turnover in the preoptic–anterior hypothalamic brain area (POAH). On day 3 after priming the noradrenaline turnover rate was reduced in the morning and increased in the afternoon. The increase correlated with an enhanced sensitivity of the LH secretory system to progesterone. The antioestrogen MTAM blocked the OB-induced sensitization of LH release to the stimulatory action of progesterone and interfered with the stimulatory long-term effect of oestradiol on hypothalamic noradrenaline turnover. The data strongly support the view that the oestrogen-induced afternoon increase of noradrenaline turnover in the POAH represents a pre-requisite for the induction of LH surges. The stimulatory effect of oestradiol on hypothalamic noradrenaline turnover seems to be mediated by a classical oestrogen receptor mechanism. J. Endocr. (1985) 106, 37–42


1997 ◽  
Vol 154 (2) ◽  
pp. 241-248 ◽  
Author(s):  
C Aurich ◽  
J Lange ◽  
H-O Hoppen ◽  
J E Aurich

Abstract The aim of this study was to investigate the influence of oestradiol, melatonin and season on the opioid regulation of LH and prolactin release. Effects of the opioid antagonist naloxone (0·5 mg/kg) on LH and prolactin secretion were determined in ovariectomized pony mares. In experiment 1, mares in January (n=6) were pretreated with oestradiol benzoate (5 μg/kg) for 20 days. In experiment 2, beginning in May, mares (n=7) received melatonin (15 mg) for 15 days and subsequently a combination of melatonin plus oestradiol for 20 days. In experiment 3, beginning in May, mares (n=6) were pretreated with oestradiol for 30 days, left untreated for 12 days and then given melatonin for 35 days. In all experiments the animals were injected with the opioid antagonist naloxone and saline on 2 consecutive days prior to treatment. In experiment 1, animals received naloxone and saline on days 10 and 11 and 20 and 21 following oestradiol treatment. In experiment 2, naloxone and saline were administered on days 15 and 16 following melatonin treatment and on days 10 and 11 and 20 and 21 of melatonin plus oestradiol treatment. In experiment 3, the animals received naloxone and saline on days 10 and 11, 20 and 21 and 30 and 31 of oestradiol treatment, prior to melatonin treatment and on days 15 and 16, 25 and 26 and 35 and 36 following melatonin. In January (experiment 1), naloxone evoked a significant (P<0·05) LH release at all times, however the LH increment in response to naloxone increased during oestradiol pretreatment (P<0·05) During the breeding season (experiments 2 and 3), naloxone induced a significant (P<0·05) increase in plasma LH concentrations when mares had not been pretreated with oestradiol or melatonin and after oestradiol pretreatment. Basal LH concentrations and the LH increment in response to naloxone increased significantly (P<0·05) during the 30-day oestradiol pretreatment. Melatonin decreased the naloxone-induced LH release and the LH release in response to naloxone and saline no longer differed after 25 and 35 days of melatonin pretreatment. When melatonin was given together with oestradiol for 20 days, again a significant (P<0·05) LH release in response to naloxone occurred. Prolactin release was significantly (P<0·05) increased by naloxone when mares had been pretreated with only melatonin. The opioid antagonist did not affect prolactin release in mares that had not been pretreated or received oestradiol either alone or in combination with melatonin. In conclusion, in long-term ovariectomized mares, opioids inhibit LH secretion independent from ovarian factors. This opioid inhibition of LH secretion is enhanced by oestradiol and reduced by melatonin. Although short-term melatonin treatment in-activates the opioid regulation of LH release, a prolonged influence of melatonin as occurs in winter does not prevent activation of the opioid system. This indicates that effects of melatonin on the opioid regulation of LH release change with time. An opioid inhibition of prolactin secretion is activated by melatonin given for 15–35 days but is lost under the prolonged influence of a short-day melatonin signal in winter. Journal of Endocrinology (1997) 154, 241–248


1983 ◽  
Vol 102 (2) ◽  
pp. 196-204 ◽  
Author(s):  
G. A. Schuiling ◽  
N. Pols-Valkhof ◽  
T. R. Koiter

Abstract. The LH releasing activities of LRH and the LRH-analogue buserelin® (HOE 766; (D-Ser (But)6-LRH(1–9)nona peptide-ethylamide) were compared in intact and short- and long-term castrated male rats, pre-treated (either 1 or 3 days) with oestradiol benzoate (EB) or oil. LRH and buserelin were infused iv at the constant rate of 104 ng/h for 21 h. Blood samples were taken from an intracarotid cannula. LH responses were judged on the basis of the mean maximal height of the LH concentration (MH; ng LH/ml plasma) and a parameter of total LH release, i.e. the area under the curve of LH concentrations plotted against time ('area under the curve', AUC; expressed in 'area units'). The release efficiency of LRH and buserelin, E (see for a definition: Materials and Methods), which informs on the total quantity of LH released in relation to pituitary LH content, was calculated by dividing the AUC × 100 by the pituitary LH content at the beginning of stimulation. Maximal plasma LH concentrations were observed between t= 1.5 and t=3 h after LRH and between t= 1.5 and t=9 after buserelin treatment. Both with LRH and buserelin the rise of LH secretion was greater the longer the animals were castrated and/or pre-treated with EB. The buserelin-induced LH response (with the exception of the responses induced in the EB-pre-treated, 4-weeks castrated rat) were about 2–2.5 times higher (MH) and larger (AUC) than the corresponding LRH-induced responses. The buserelin/LRH potency ratio, therefore, is about 2–2.5. EB-pre-treatment did not change the pituitary LH content. It therefore enhanced the efficiency of release of LH of both LRH and buserelin. Castration, on the other hand, caused an increase of the pituitary LH content: after 4 weeks it was raised by a factor 4. Since, however, the LH responses induced by LRH and buserelin were proportionally higher and larger, castration did not significantly change the efficiency of LH release. The results indicate that the efficiency of LH release can be changed by changes in the endocrine environment in the experimental animals, whilst for the magnitude of LH responses the pituitary LH content is also important. It is therefore suggested that the responsiveness of the pituitary gland to LRH (and agonistic analogues) is determined by (1) the state of the LH secretion mechanism and (2) the pituitary LH content.


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