Differential responses of hypothalamic LHRH-I and -II to castration and gonadal steroid or tamoxifen treatment in cockerels

1990 ◽  
Vol 125 (1) ◽  
pp. 139-146 ◽  
Author(s):  
S. C. Wilson ◽  
R. T. Gladwell ◽  
F. J. Cunningham

ABSTRACT Changes in the hypothalamic contents of LHRH-I and LHRH-II were determined in intact and castrated cockerels injected i.m. with gonadal steroids or tamoxifen. An increase in the plasma concentration of LH after castration was accompanied by a significant increase in the content of LHRH-I in the posterior hypothalamus (including the mediobasal hypothalamus and median eminence) which was reversed by oestradiol benzoate given on days 14 and 15 after castration. Under similar circumstances, testosterone propionate did not modify the hypothalamic content of LHRH-I, even though both steroids reduced the plasma concentrations of LH to levels below those of intact cockerels. Treatment of intact cockerels with oestradiol benzoate significantly increased the content of LHRH-I in the posterior hypothalamus, whilst testosterone propionate was again without effect. Tamoxifen significantly raised the plasma concentration of LH in intact cockerels and partially antagonized the suppressive effect of oestradiol benzoate and testosterone on LH secretion in castrated cockerels. However, an anti-oestrogenic effect of tamoxifen on the hypothalamic content of LHRH-I was not demonstrated. There was no evidence of any changes in the hypothalamic content of LHRH-II after castration, with or without gonadal steroid replacement. A change in the hypothalamic content of LHRH-I in response to manipulation of the steroid environment would imply an involvement of this peptide in the mechanism by which gonadal steroids regulate the release of LH. The absence of changes in the hypothalamic content of LHRH-II in the same circumstances suggest that it is not directly involved in the control of LH secretion by the gonadal steroid negative feedback loop. Journal of Endocrinology (1990) 125, 139–146

1991 ◽  
Vol 130 (3) ◽  
pp. 457-462 ◽  
Author(s):  
S. C. Wilson ◽  
R. T. Gladwell ◽  
F. J. Cunningham

ABSTRACT Diurnal changes of LH secretion in sexually immature hens of 9, 11, 13 and 15 weeks of age consisted of 25–40% increases in the mean concentrations of LH in plasma between 15.00 and 18.00 h, i.e. between 2 h before and 1 h after the onset of darkness. During this time there was a tendency for the mean contents of LHRH-I in the anterior hypothalamus and posterior hypothalamus to increase by 21–74% and 20–56% respectively. In hens of 9 and 15 weeks, diurnal changes in the plasma concentration of LH closely paralleled those of LHRH-I content in the posterior hypothalamus. In contrast, the diurnal rhythm of LH secretion in hens of 11 and 13 weeks was more marked and plasma concentrations of LH continued to rise steeply between 18.00 and 21.00 h, i.e. between 1 and 4 h after the onset of darkness. At 11 weeks, this was associated with a reduction (P<0·01) in the contents of LHRH-I and LHRH-II, particularly in the anterior hypothalamus. In laying hens, a diurnal decline (P<0·01) in the plasma concentration of LH between 1 and 4 h after the onset of darkness was preceded by a fall (P<0·05) in the content of LHRH-I in the posterior hypothalamus and in the total hypothalamic content of LHRH-II (P<0·01). In all groups of hens, irrespective of the times of day at which tissue was taken, significant (P<0·05–<0·001) correlations between the contents of LHRH-I and LHRH-II in the anterior hypothalamus were observed. It is concluded that a diurnal rhythm of release of LHRH-I may drive the diurnal rhythm of LH secretion. Thus, in sexually immature hens of 9 and 15 weeks and laying hens in which diurnal changes in plasma LH were small there were parallel changes in the content of LHRH-I in the posterior hypothalamus. However, where the plasma concentration of LH was increased substantially, as at 11 weeks, there was a decline in the hypothalamic contents of LHRH-I. A simultaneous fall in the hypothalamic content of LHRH-II raises the possibility of a causal relationship between the activities of LHRH-II, LHRH-I and the release of LH. Journal of Endocrinology (1991) 130, 457–462


1983 ◽  
Vol 99 (1) ◽  
pp. 23-29 ◽  
Author(s):  
I. J. Clarke

The effects of tamoxifen on peripheral plasma concentrations of gonadotrophins were studied in ovariectomized ewes. First, ovariectomized ewes were injected (i.m.) with 10 mg tamoxifen citrate/day for 4 days which caused a significant reduction in plasma LH concentrations within 4 days and plasma FSH concentrations within 1 day of the commencement of treatment. Further groups of ovariectomized ewes were then injected (i.m.) with two injections of 10 mg tamoxifen citrate 6 h apart or 20 μg oestradiol benzoate (OB) or tamoxifen citrate plus OB or oil. Tamoxifen treatment caused a reduction in plasma LH and FSH concentrations within 6 h. In four of our ewes receiving OB, a surge in LH secretion was observed; a similar response was observed in two out of four ewes given the combination of tamoxifen citrate and OB. No LH surge was seen in ovariectomized ewes given tamoxifen alone. These results show that tamoxifen reduces plasma gonadotrophin levels in ovariectomized ewes suggesting it is an oestrogen agonist in the sheep pituitary gland. A partial oestrogen antagonist action of tamoxifen is similarly suggested by its ability to block the oestrogen-induced LH surge in some ovariectomized ewes. Since tamoxifen consistently lowers plasma gonadotrophin levels in ovariectomized ewes this could result from action via oestrogen receptors or by central nervous system, non-oestrogen receptor-mediated effects.


1988 ◽  
Vol 118 (2) ◽  
pp. 193-197 ◽  
Author(s):  
H. Dobson ◽  
S. A. Essawy ◽  
M. G. S. Alam

ABSTRACT Stress is known to result in lowered female reproductive efficiency. The objective of this study was to examine how increased pituitary-adrenal activity may influence gonadotrophin release in anoestrous ewes. Various doses (0·06–1·0 mg) of a synthetic adrenocorticotrophic hormone (ACTH(1–24)) preparation were injected into ewes 30 min or 3 h before an i.v. injection of 500 ng gonadotrophin-releasing hormone (GnRH). The LH response to GnRH given 30 min after ACTH(1–24) was similar to that after GnRH alone, whereas the response 3 h after ACTH(1–24) was significantly lower, irrespective of the dose of ACTH(1–24). At 30 min and 3 h after ACTH(1–24) the concentrations of cortisol exceeded 50 nmol/l compared with baseline values of < 10 nmol/l. The effect of ACTH(1–24) on oestradiol-induced LH release was also examined. Those ewes receiving 0·8 mg ACTH(1–24) depot and 50 μg oestradiol benzoate simultaneously had a preovulatory-type increase in LH 14–20 h later, similar to when oestradiol benzoate was given alone. None of the ewes receiving an additional 0·8 mg ACTH(1–24) depot 10 h after oestradiol benzoate had increases in LH concentration. The cortisol concentrations in all ewes receiving either one or two injections of ACTH(1–24) were > 35 nmol/l at 10 h after the oestradiol injection. However, concentrations of progesterone increased from 0·9 ± 0·3 (s.e.m.) nmol/l at the time of the second ACTH(1–24) injection to 2·1 ±0·3 nmol/l after 2 h. In summary, it would appear that the suppressive effect of ACTH(1–24) on LH secretion induced by GnRH or oestradiol in the anoestrous ewe is not dependent on increased plasma concentrations of cortisol. J. Endocr. (1988) 118, 193–197


1983 ◽  
Vol 99 (2) ◽  
pp. 301-310 ◽  
Author(s):  
S. C. Wilson ◽  
P. G. Knight ◽  
F. J. Cunningham

Treatment of intact cockerels with the synthetic antioestrogen tamoxifen caused a significant increase in the plasma concentration of LH. In contrast, passive immunization with an antiserum raised against oestradiol-17β did not lead to an increase in plasma LH. A pronounced depressive effect of injections of 0·1 mg testosterone propionate (TP) or 0·1 mg oestradiol benzoate (OB) on plasma concentrations of LH was prevented by tamoxifen. Furthermore, a pronounced rise in the concentration of LH releasing hormone in the posterior hypothalamus after the injection of cockerels with OB was completely inhibited by tamoxifen. Neither 0·1 nor 0·5 mg androstenedione modified the concentration of LH in plasma. A dose of 0·05 mg TP, which failed to depress the concentration of LH in plasma of intact cockerels, caused a marked fall in plasma LH in castrated cockerels. Tamoxifen itself exhibited weak oestrogen agonist activity in castrated cockerels by causing a reduction in the concentration of LH in plasma. However, tamoxifen prevented any further depressive effect on LH resulting from the injection of TP. These findings suggest that testosterone exerts an inhibitory influence on LH secretion at the central neural level, partially at least, by means of the product of its aromatization, oestradiol-17β.


1971 ◽  
Vol 50 (1) ◽  
pp. 97-113 ◽  
Author(s):  
J. B. HUTCHISON

SUMMARY To determine whether the display of male courtship behaviour depends on the action of androgen on discrete areas of the brain, single crystalline implants of testosterone propionate (TP) (mean weight 40 μg) were positioned unilaterally in the brains of castrated male Barbary doves. Implants in the preoptic, anterior hypothalamic and lateral hypothalamic areas induced the full courtship display consisting of chasing, bowing and nestsoliciting. None of these behaviour patterns was re-established at precastration levels measured in terms of duration of display. Durations of courtship displayed by implanted males were similar to those induced by daily intramuscular injections of TP (300 μg/day × 15) into castrated birds. The effectiveness of implants of TP into other regions of the brain could be related to their proximity to the preoptic and anterior hypothalamic regions. There were marked deficits in the pattern of courtship of castrated doves with implants in areas adjacent to the preoptic and anterior hypothalamic regions — the neostriatum intermediale, the area basalis, and posterior hypothalamus; implants more distantly placed in the paleostriatum primitivum and lateral forebrain bundle area did not induce courtship behaviour. Cholesterol implants (59 μg) and blank implant tubing in the preoptic and anterior hypothalamic areas did not affect behaviour. The results obtained were not specific for TP implants; chasing and nest-soliciting displays were also induced by either testosterone implants (51 μg) or oestradiol-17β monobenzoate implants (47 μg). In both cases, the courtship display lacked bowing. It is concluded that the preoptic and anterior hypothalamic areas are directly sensitive to testosterone and that these areas are associated with the control of courtship behaviour.


1984 ◽  
Vol 102 (2) ◽  
pp. 133-141 ◽  
Author(s):  
R. Bhanot ◽  
M. Wilkinson

ABSTRACT We have attempted to clarify the physiological involvement of endogenous opiates in the steroid-mediated control of gonadotrophin release. Our studies showed that there was an acute reduction in the inhibitory effects of endogenous opiates on LH and FSH release following gonadectomy in the rat. This was indicated by a significant reduction in the ability of naloxone to stimulate serum LH/FSH levels (sampled at 15 min) in 26-day-old female rats 48 h after ovariectomy. Luteinizing hormone was highly sensitive to the inhibitory effects of the synthetic met-enkephalin analogue, FK 33-824, at this time (sampled at 90 min). An unexpected observation was that long-term absence of gonadal steroids also disrupted the ability of exogenous opiates, FK 33-824 and morphine, to influence LH release. This was seen as an inability of FK 33-824 (1·0 or 3·0 mg/kg) to inhibit LH secretion. The effects of gonadectomy on opiate control of LH occurred at all developmental stages and were not due to a disruption of sexual maturation. Opiate involvement in prolactin secretion did not appear to be adversely affected by an absence of gonadal steroids. Another novel aspect of this work was that the opiatergic component in the control of gonadotrophin secretion could be reinstated in long-term gonadectomized rats by treatment with oestradiol benzoate or testosterone propionate. Similarly, priming with increasing dosages of oestradiol benzoate which resulted in progressively lower LH levels gave larger naloxone responses. This steroid–opiate interdependency suggests that the negative feedback influence of gonadal steroids on LH secretion is conveyed, in part, by hypothalamic opiate peptides. Our results therefore provide a neurochemical basis for gonadal steroid negative feedback. J. Endocr. (1984) 102, 133–141


1990 ◽  
Vol 127 (3) ◽  
pp. 487-496 ◽  
Author(s):  
S. C. Wilson ◽  
R. A. Chairil ◽  
F. J. Cunningham ◽  
R. T. Gladwell

ABSTRACT The contents of LHRH-I and -II in the anterior hypothalamus and posterior hypothalamus (including the mediobasal hypothalamus and median eminence) were measured at 90, 180 and 360 min after the i.m. injection of laying hens with progesterone. Whilst no changes were observed in the content of LHRH-I in the anterior hypothalamus, LHRH-I in the posterior hypothalamus tended to fall at 90 and 180 min after injection of progesterone in hens maintained on 16 h light:8 h darkness (16L:8D) and 8L:16D respectively. Pretreatment of laying hens with tamoxifen significantly increased the hypothalamic contents of LHRH-I and -II, raised the basal plasma concentration of LH and modified the LH response to progesterone injection. In hens in which tamoxifen prevented an increase in the plasma concentration of LH after progesterone injection, the content of LHRH-I in the posterior hypothalamus remained unchanged. In contrast, in hens in which progesterone stimulated a steep increase in LH within 90 min, there was a pronounced and significant fall in LHRH-I content of the posterior hypothalamus. No change in the hypothalamic content of LHRH-II was observed during the progesterone-induced surge of LH until plasma concentrations had attained maximal values or started to decline. Then, in hens maintained on 16L:8D, a significant fall in the content of LHRH-II in the anterior hypothalamus was found at both 180 and 360 min after injection with progesterone. Tests in vitro and in vivo of the responsiveness of the pituitary gland to synthetic LHRH-I and -II revealed no change at 90 min after injection of laying hens with progesterone, when plasma concentrations of LH were increasing, but a pronounced reduction when plasma LH concentrations were maximal or falling. These results suggest that LHRH-I mediates in the progesterone-induced increase in the plasma concentration of LH. Although the subsequent decline in plasma LH was associated with a reduced responsiveness of the pituitary gland to LHRH, a significant correlation between the contents of LHRH-I and -II in the anterior hypothalamus and a fall in the hypothalamic content of LHRH-II when plasma LH was maximal or declining allows the possibility of an involvement of this peptide in the neuroendocrine events preceding ovulation. Journal of Endocrinology (1990) 127, 487–496


1980 ◽  
Vol 86 (2) ◽  
pp. 251-261 ◽  
Author(s):  
J. BALTHAZART ◽  
J. D. BLAUSTEIN ◽  
M. F. CHENG ◽  
H. H. FEDER

A cytoplasmic progestin receptor has been characterized in the brain of castrated ring doves using an in-vitro assay that measures the binding of a synthetic progestin, [3H]17α,21-dimethyl-19-nor-pregna-4,9-diene-3,20-dione(promegestone; R5020). The affinity of the receptor was similar in both the hyperstriatum and the hypothalamus (Kd≃4 × 10−10 mol/l). Its concentration was higher in the anterior hypothalamus–preoptic area (63 ± 4 fmol/mg (s.e.m.) protein) than in other brain regions (posterior hypothalamus, 33 ± 5; hyperstriatum, 28 ± 3; midbrain, 17 ± 4 fmol/mg protein; n = 7). Progesterone and R5020 competed well for binding but oestradiol and 5β-dihydrotestosterone did not. Corticosterone and, to a lesser extent, testosterone and 5α-dihydrotestosterone competed for binding but much higher concentrations were required than for progestins. Injections of testosterone (200 pg testosterone propionate daily for 7 days) significantly increased the concentration of progestin receptors in the anterior and posterior hypothalamus without having any significant effect on other brain areas. Shorter treatment, lasting for 2 days, with testosterone propionate (200 μg daily), 5α-dihydrotestosterone (200 μg daily) or oestradiol benzoate (50 μg daily) did not always cause this increase but seven injections of oestradiol benzoate (50 pg daily for 7 days) were even more effective than seven injections of testosterone propionate (200 μg daily for 7 days). These data suggested that the sensitivity to progesterone of the brain of the bird changes as a consequence of increases in the level of testosterone in the circulation.


1975 ◽  
Vol 66 (2) ◽  
pp. 183-193 ◽  
Author(s):  
D. GUPTA ◽  
K. RAGER ◽  
J. ZARZYCKI ◽  
M. EICHNER

SUMMARY Plasma concentrations of LH, FSH, testosterone and dihydrotestosterone (DHT) have been measured in normal sexually maturing male rats from the age of 16–90 days. Between 16 and 25 days plasma testosterone levels were low, but rose suddenly on day 26. A similar increment occurred at the same time in plasma DHT levels, but this steroid reached its peak concentration later than testosterone. Plasma LH levels rose steadily from day 25 onwards, reaching their highest values on day 30. A marked increase in FSH levels was found on day 16, and a peak was reached on day 33 followed by a decline to a level characteristic of the adult. In addition, plasma levels of all these hormones were estimated in the male animals at various stages of development after orchidectomy and cryptorchidism. Four days after operation, the plasma levels of LH and FSH in the orchidectomized animals reached higher levels than those found in the intact animals, indicating the existence of a dynamic feedback relationship before puberty between gonadal steroids and pituitary gonadotrophic secretion. However, results from the experimental bilaterally cryptorchid animals, suggested that the gonadal steroid–gonadotrophic feedback relationship could not be the only factor initiating puberty.


1978 ◽  
Vol 78 (3) ◽  
pp. 329-342 ◽  
Author(s):  
F. ELSAESSER ◽  
N. PARVIZI ◽  
F. ELLENDORFF

The effects of gonadal secretions on the release of LH and the stimulation of LH secretion by oestradiol have been investigated in newborn male and female miniature pigs; the differences in the feedback action of testosterone in newborn and pubertal male pigs were also studied. Hemi-orchidectomy or orchidectomy of 1-week-old pigs had no effect on the level of LH in the plasma; total orchidectomy significantly reduced the levels of testosterone (P<0·01) and progesterone (P<0·05). In female pigs ovariectomized at 1 week of age, the concentration of LH in the plasma decreased, with a strong negative correlation between the level of LH and age (r = −0·41; P < 0·05). The plasma concentration of progesterone was generally low and unaffected by ovariectomy. Orchidectomy and treatment of male pigs, at 1 week of age, with testosterone (6 mg/kg body weight) had no effect on the plasma concentration of testosterone 24 h after treatment. If testosterone propionate was given rather than testosterone, the level of LH was significantly reduced (P< 0·001) 24 h after the injection and the concentration of testosterone in the plasma corresponded to that found in the intact adult male pig. Treatment with oestradiol or oestradiol benzoate did not affect the concentration of LH. Orchidectomy and treatment of pubertal male pigs with testosterone propionate resulted in a significantly (P < 0·001) higher concentration of testosterone in the plasma, compared with newborn pigs treated similarly, but the level of LH was unchanged. This suggests that there is a more rapid rate of clearance of testosterone in the newborn than in the pubertal male miniature pig and that the negative feedback of testosterone is not mediated by aromatization in the newborn animal and it declines before or during puberty. Treatment of newborn intact male and female and gonadectomized male pigs with oestradiol benzoate produced similar variations in the plasma level of oestradiol in all groups of animals. In the female pigs, however, a surge-like release of LH was observed 60–72 h after the injection of oestradiol benzoate, suggesting that the stimulatory feedback mechanism can operate soon after birth and that the response is sexually dimorphic.


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