Blockage of gonadotropin-induced first ovulation caused by thyroidectomy and its possible mechanisms in rats

1998 ◽  
Vol 275 (3) ◽  
pp. E380-E385 ◽  
Author(s):  
Kazuhiro Tamura ◽  
Minoru Hatsuta ◽  
Gen Watanabe ◽  
Kazuyoshi Taya ◽  
Hiroshi Kogo

To determine the role of the thyroid gland on the ovarian functions during the initiation process of puberty, we examined the effects and its mechanisms of hypothyroidism on the first ovulation induced by equine chorionic gonadotropin (eCG) in immature female rats. Animals were thyroidectomized on day 22 and were injected with 5 IU of eCG on day 26 to induce the first ovulation on day 29. The number of antral follicles that secrete inhibin and the ovarian weight were significantly increased in thyroidectomized rats (Tx rats) 48 h after eCG treatment compared with those in non-Tx rats. However, thyroidectomy (Tx) significantly suppressed the rates of ovulating animals on day 29. The blockage of ovulation in Tx rats was recovered by administration of human chorionic gonadotropin or luteinizing hormone (LH)-releasing hormone (LHRH) on day 28. Inhibition of serum LH (not follicle-stimulating hormone) levels induced by Tx was almost restored to control levels by injection of LHRH. A significant increment in prolactin levels in Tx rats was also observed on day 28. The present data indicate that Tx before puberty in female rats causes the blockage of the first ovulation and that the inhibitory effects on ovulation are mainly due to the reduction in the preovulatory LH surge, which is partially mediated through an inhibition of LHRH action on the secretion of LH.

1981 ◽  
Vol 241 (6) ◽  
pp. E460-E464
Author(s):  
J. R. Lorenzen ◽  
J. A. Ramaley

Serum gonadotropin levels were measured 12, 24, and 48 h after gonadectomy in male and female rats (ages, 22--60 days) to assess when during development the rate of rise of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) after castration approximates that seen in the gonadectomized adult. In females serum LH levels 48 h after ovariectomy were increased above sham levels only when the ovaries were removed prior to vaginal opening. Ovariectomy on the day of vaginal opening or at older ages resulted in no increase in LH levels by 48 h after surgery. Serum FSH levels at 24 and 48 h after ovariectomy declined with increasing age at the time of ovariectomy. In males serum LH levels at 48 h after castration increased with increasing age at the time of gonadectomy. Serum FSH levels at either 12, 24, or 48 h after orchidectomy did not change appreciably with age at the time of surgery. It is concluded that the acute pituitary secretion of gonadotropins after removal of testes in the immature male resembles that seen in the mature male early in the course of the development of sexual maturity. In contrast, the acute pituitary secretion of gonadotropins after removal of the ovaries in the immature female does not resemble that seen in the ovariectomized adult until she is mature and capable of ovulating. Thus, the observed delay in the rise of LH seen in ovariectomized adults may be a function of some aspect of the hormonal changes associated with the estrous cycle.


1970 ◽  
Vol 48 (4) ◽  
pp. 527-539 ◽  
Author(s):  
H. F. CARRER ◽  
S. TALEISNIK

SUMMARY Different regions of the midbrain were stimulated by electrolytic deposition of iron from stainless steel unipolar electrodes. Electrochemical stimulation of the ventral tegmental area (VTA), the raphe nuclei or the peri-aqueductal grey in rats in pro-oestrus was effective in preventing spontaneous ovulation. No blockade of ovulation was observed by stimulating other mesencephalic structures. After stimulation in the VTA there was a significant decrease of the elevated serum levels of luteinizing hormone (LH) found after an injection of progesterone into pro-oestrous rats or into ovariectomized—oestrogen-primed animals. In contrast, electrochemical stimulation of the dorsal mesencephalic tegmentum, lateral and inferior to the peri-aqueductal grey, in rats in which spontaneous ovulation had been blocked by continuous illumination, resulted in an ovulatory response. Serum LH was found to increase in gonadectomized—oestrogen-treated male and female rats after stimulating this area. No significant changes in serum follicle-stimulating hormone were found after stimulation in the ventral or dorsal tegmentum. It is concluded that both stimulatory and inhibitory influences on the release of gonadotrophin can be evoked by stimulating mesencephalic structures. The stimulatory and inhibitory effects could depend on the activation of noradrenergic and serotoninergic systems, respectively.


1993 ◽  
Vol 16 (5) ◽  
pp. 483-485 ◽  
Author(s):  
Hiroshi KOGO ◽  
Kotaro TAKASAKI ◽  
Satoshi TAKEO ◽  
Gen WATANABE ◽  
Kazuyoshi TAYA ◽  
...  

2019 ◽  
Vol 130 ◽  
pp. 99-102 ◽  
Author(s):  
Yves Combarnous ◽  
Julie Mariot ◽  
Lauriane Relav ◽  
Thi Mong Diep Nguyen ◽  
Danièle Klett

1973 ◽  
Vol 74 (3) ◽  
pp. 449-460 ◽  
Author(s):  
Patrick C. Walsh ◽  
Ronald S. Swerdloff ◽  
William D. Odell

ABSTRACT Serum follicle stimulating hormone (FSH) and luteinizing hormone (LH) were measured by radioimmunoassay in a group of elderly men following castration and oestrogen therapy. Prior to orchiectomy, mean serum concentrations of LH and FSH were within the normal range. Two days following castration, serum LH concentrations increased in all eight patients; higher levels of LH were subsequently measured in all but one patient after periods of time ranging from 49 to 210 days. Serum FSH levels, measured in three patients following castration, increased in a pattern parallel to LH changes. Ethinyl oestradiol (EOe) in doses ranging from 5 to 300 μg/day was administered to ten men who had been castrated 3 to 72 months earlier. Oestrogen treatment suppressed both LH and FSH in a parellel manner in nine of ten patients. LH was first suppressed to intact levels in one of eight patients treated with 20 μg/day of EOe, in two of six patients treated with 50 μg/day, and in one patient by 80 μg/day. FSH was not suppressed to precastration levels until 50 μg/day of EOe was administered; this dose suppressed three of six patients. Higher doses of EOe (150–300 μg/day) suppressed both LH and FSH to levels below the sensitivity of the assay. These data fail to demonstrate any differential effect of oestrogen on LH and FSH release.


1979 ◽  
Vol 91 (3) ◽  
pp. 591-600 ◽  
Author(s):  
Toshihiro Aono ◽  
Akira Miyake ◽  
Takenori Shioji Motoi Yasuda ◽  
Koji Koike ◽  
Keiichi Kurachi

ABSTRACT Five mg of bromocriptine was administered for 3 weeks to 8 hyperprolactinaemic women with galactorrhoea-amernorrhoea, in whom the response of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to 100 μg of iv LH-releasing hormone (LH-RH) had been evaluated. Twenty mg of conjugated oestrogen (Premarin®) was injected iv any day between the 10th and 12th day from the initiation of the treatment, and serum LH levels were serially determined for 120 h. Hyperresponse of LH with normal FSH response to LH-RH was observed in most patients. Bromocriptine treatment for 10 to 12 days significantly suppressed mean (± se) serum prolactin (PRL) levels from 65.1 ± 23.0 to 10.4 ± 2.0 ng/ml, while LH (12.6 ± 2.1 to 24.8 ± 5.9 mIU/ml) and oestradiol (40.1 ± 7.6 to 111.4 ± 20.8 pg/ml) levels increased significantly. Patients on bromocriptine treatment showed LH release with a peak at 48 h after the injection of Premarin. The mean per cent increases in LH were significantly higher than those in untreated patients with galactorrhoea-amenorrhoea between 32 and 96 h after the injection. The present results seem to suggest that the restoration of LH-releasing response to oestrogen following suppression of PRL by bromocriptine may play an important role in induction of ovulation in hyperprolactinaemic patients with galactorrhoea-amenorrhoea.


Sign in / Sign up

Export Citation Format

Share Document