IMPAIRMENT OF THE CONTROL OF GONADOTROPHIN SECRETION AFTER OESTROGEN ADMINISTRATION TO ADULT FEMALE RATS

1977 ◽  
Vol 73 (3) ◽  
pp. 497-505 ◽  
Author(s):  
K. BROWN-GRANT ◽  
M. B. TER HAAR

SUMMARY The possible occurrence of long-term changes in gonadotrophin control mechanisms following the administration of oestrogen to adult female rats has been studied. Administration of 2·5 mg oestradiol benzoate (OB) to normal female rats at 60 days of age did not result in failure of ovulation at 120 days of age but significant impairment of the LH and FSH responses to progesterone after ovariectomy and oestrogen priming was observed at 160–180 days of age. Treatment with the same dose of OB at 60 days of rats injected with 10 μg testosterone propionate on Day 4 of postnatal life resulted in an increased incidence of failure of ovulation at 120 though not at 150 days of age but did not further impair the already reduced gonadotrophin response to progesterone at 160–180 days of age. Removal of the ovaries at 60 days of age did not modify the effects of oestrogen given at 60 days of age in either group nor did ovariectomy at 60 days improve the response of neonatally androgen-treated rats to progesterone at 160–180 days of age. The increases in plasma prolactin and TSH levels in response to oestrogen priming after ovariectomy were not affected in any of the experimental groups. The administration of a long-acting oestrogen preparation (oestradiol cyclopentyl propionate, 2·5 mg at 60 days of age) to normal female rats suppressed ovulation and depressed plasma LH and FSH concentrations for at least 90 days; anterior pituitary weights were greatly increased and plasma prolactin concentrations were very high.

1982 ◽  
Vol 95 (2) ◽  
pp. 207-213 ◽  
Author(s):  
Patrizia Limonta ◽  
Roberto Maggi ◽  
Luciano Martini ◽  
Flavio Piva

Thermal lesions were placed in the subcommissural organ (SCO) of female rats with normal cycles and long-term ovariectomized rats. In normal female rats SCO lesions disrupted the oestrous cycle in more than half of the animals, the majority of which entered a state of prolonged dioestrus. In these animals, serum gonadotrophin levels were similar to those of rats with regular cycles on day 2 of dioestrus. In animals in which the oestrous cycle was maintained, a delayed LH surge occurred on the day of pro-oestrus and the pro-oestrous FSH surge was absent. The usual increase in FSH on the day of oestrus was present. Lesions in the SCO did not change the high gonadotrophin levels typical of ovariectomized animals. These results suggested that the SCO may play a role in the control of the cyclic but not the tonic release of the gonadotrophins. In particular, it appears that the SCO might be involved in the regulation of the hypersecretion of FSH during the day of pro-oestrus.


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


2009 ◽  
Vol 9 (3) ◽  
pp. 409-416 ◽  
Author(s):  
Charlotte H. Søgaard ◽  
Carl Christian Danielsen ◽  
Eivind B. Thorling ◽  
Lis Mosekilde

1981 ◽  
Vol 97 (2) ◽  
pp. 181-185 ◽  
Author(s):  
Daniel M. Linkie ◽  
Jacob Furth ◽  
Diane Kourelakos

Abstract. The patterns of gonadotrophin secretion in intact controls and in male and female rats castrated for up to 36 months were established utilizing specific radioimmunoassay methods. Plasma LH increased 14– 16-fold and FSH rose 4–8-fold in rats of either sex in the first 30 days following gonadectomy. The subsequent 30 day interval showed an additional 76% increase of LH in both sexes and increases in FSH of 32 and 61% in males and females, respectively. These levels were maintained for an additional 34 months. The number of hypophyseal gonadotrophin containing cells, studied by immunohistochemical localization techniques, increased following gonad removal in a pattern similar to that for the circulating hormones. Development of gonadotrophin secreting tumours did not correlate with plasma gonadotrophin concentrations which suggests that the gonadotropes are uniquely resistant to tumourogenesis unlike mammotropes, thyrotropes, and corticotropes.


1977 ◽  
Vol 73 (3) ◽  
pp. 455-462 ◽  
Author(s):  
S. R. HENDERSON ◽  
CHRISTINE BAKER ◽  
G. FINK

SUMMARY The effect of oestradiol-17β (administered in Silastic capsules) on gonadotrophin secretion in long-term gonadectomized rats has been investigated. In female rats, a daily afternoon surge of LH occurred which could be blocked by administering sodium pentobarbitone at 13.00 h. This, together with the fact that there was no significant difference between the LH-response to LH-releasing factor in the morning compared with the afternoon, supports the view that the LH surges are due to a neural rhythm. There was no significant diurnal variation in plasma FSH concentration, but an apparent diurnal variation was disclosed by administering sodium pentobarbitone on alternate days. There was no diurnal variation in plasma gonadotrophin concentrations in male animals implanted with an oestradiol capsule, or in animals of either sex bearing empty capsules.


2012 ◽  
Vol 303 (6) ◽  
pp. R651-R657 ◽  
Author(s):  
Kirk W. Evanson ◽  
Audrey J. Stone ◽  
Enoch Samraj ◽  
Tyler Benson ◽  
Rhonda Prisby ◽  
...  

The effects of estradiol on neuropeptide Y (NPY) neurotransmission in skeletal muscle resistance vessels have not been described. The purpose of this study was to determine the effects of long-term estradiol supplementation on NPY overflow, degradation, and vasoconstriction in gastrocnemius first-order arterioles of adult female rats. Female rats (4 mo; n = 34) were ovariectomized (OVX) with a subset ( n = 17) receiving an estradiol pellet (OVE; 17β-estradiol, 4 μg/day). After conclusion of the treatment phase (8 wk), arterioles were excised, placed in a physiological saline solution (PSS) bath, and cannulated with micropipettes connected to albumin reservoirs. NPY-mediated vasoconstriction via a Y1-agonist [Leu31Pro34]NPY decreased vessel diameter 44.54 ± 3.95% compared with baseline; however, there were no group differences in EC50(OVE: −8.75 ± 0.18; OVX: −8.63 ± 0.10 log M [Leu31Pro34]NPY) or slope (OVE: −1.11 ± 0.25; OVX: −1.65 ± 0.34% baseline/log M [Leu31Pro34]NPY). NPY did not potentiate norepinephrine-mediated vasoconstriction. NPY overflow experienced a slight increase following field stimulation and significantly increased ( P < 0.05) over control conditions in the presence of a DPPIV inhibitor (diprotin A). Estradiol status did not affect DPPIV activity. These data suggest that NPY can induce a moderate decrease in vessel diameter in skeletal muscle first-order arterioles, and DPPIV is active in mitigating NPY overflow in young adult female rats. Long-term estradiol supplementation did not influence NPY vasoconstriction, overflow, or its enzymatic breakdown in skeletal muscle first-order arterioles.


1985 ◽  
Vol 104 (2) ◽  
pp. 299-307 ◽  
Author(s):  
D. J. S. Sirinathsinghji ◽  
M. Motta ◽  
L. Martini

ABSTRACT Studies were undertaken using the opiate receptor antagonist naloxone to examine the hypothesis that endogenous opiates may have a restraining effect on prepubertal gonadotrophin secretion and may be involved in the maturation of the central nervous system mechanisms regulating the onset of puberty in the female rat. Naloxone (2·5 mg/kg) administered intraperitoneally every 6 h to female rats from day 1 to day 10 of postnatal life significantly (P <0·001) advanced the age of onset of puberty assessed in terms of the day of vaginal opening and first oestrus (32·3 ± 0·2 vs 40·8 ± 0·4 days in control saline-treated animals). Animals so treated with naloxone showed significantly (P < 0·001) higher levels of FSH (761·4 ± 87·6 vs 483·8± 57·2 μg/l in control animals) and LH (562·8 ± 57·4 vs 351·3 ± 43·3 μg/l in control animals) at the first late pro-oestrus and a significantly (P < 0·001) higher number of ova released at first oestrus (12·4 ± 0·4 vs 8·1±0·3 in controls). Body weight at first oestrus was significantly (P <0·001) lower in the naloxone-treated animals, an indication that these animals were much younger. The weights (per 100 g body wt) of the ovaries and uteri at the first oestrus were significantly (P <0·01) higher in the naloxone-treated rats than in the controls. However, there were no significant differences in the weights of the adrenals and anterior pituitary glands between the two groups of animals. A study of the cyclic patterns of the neonatally naloxone-treated animals performed for 15 consecutive cycles after the first oestrus showed normal 4- or 5-day cycles similar to those occurring in the saline-treated animals. The lengths of the first and second cycles in the naloxone-treated animals were not significantly different from controls. No significant differences in body weight or in organ weights at oestrus or in the levels of LH and FSH determined during the various stages of the oestrous cycle were found between naloxone- and saline-treated animals when these parameters were examined at 3 months of age. Naloxone had no effect on onset of puberty when administered during the other stages of prepubertal life. The mechanisms by which naloxone acts specifically during the neonatal period to induce precocious puberty are at present not known but are being investigated; they may be related to naloxone-induced alterations in the inhibitory synaptic arrangements between opiatergic and gonadotrophin-releasing hormone (GnRH) neurones, with a resulting decrease in the inhibitory influence exerted by endogenous opioids on GnRH neurones during this period of intense neurological development. The results suggest that the endogenous opiate peptides could play a key role in the central mechanisms which trigger the onset of puberty in the female rat. J. Endocr. (1985) 104, 299–307


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