OESTROGEN AND THE CONTROL OF GONADOTROPHIN SECRETION IN THE IMMATURE RAT

1974 ◽  
Vol 63 (2) ◽  
pp. 285-298 ◽  
Author(s):  
F. DÖCKE ◽  
G. DÖRNER

SUMMARY Experiments were performed in female Wistar rats on the mode of action of oestrogen in affecting gonadotrophin secretion during infancy. Using an improved implantation method, former findings on a hypophysial site of oestrogen action in the Hohlweg effect were confirmed. The sensitivity to the ovulation-inducing effect of oestradiol benzoate (OB) increased as the rats approached the age of natural puberty. The first spontaneous ovulation could be suppressed by intrahypophysial, but not by intrahypothalamic, progesterone implants. A single s.c. injection or intracranial administration of OB at 25 or 26 days of age, although leading to premature vaginal opening (VO) and, in some of the animals, to one ovulation, did not induce true precocious puberty. To accelerate the onset of puberty, 0·05 μg OB/100 g body wt had to be injected daily from 5 days of age to VO, or from day 5 to day 10 and, additionally, from day 26 to VO. After long-term oestrogen treatment, the gonadotrophin-inhibiting effect of OB implanted into the middle hypothalamus from 26 to 34 days of age was significantly reduced in comparison with untreated control rats. A final experiment demonstrated that the first ovarian cycle was not prolonged after neonatal ovariectomy and implantation of ovaries at 24, 28 or 32 days of age. The results indicate that similar neurohormonal mechanisms are operational at the first pubertal and at later cyclic ovulations. They also indicate that the maturation of the gonadotrophin-controlling mechanisms continues during infancy in the absence of ovarian steroids. It can be accelerated in Wistar rats by long-term, but not by short-term prepubertal oestrogen treatment.

1985 ◽  
Vol 110 (3) ◽  
pp. 329-337 ◽  
Author(s):  
G. A. Schuiling ◽  
H. Moes ◽  
T. R. Koiter

Abstract. The effect of pretreatment in vivo with oestradiol benzoate on in vitro secretion of LH and FSH was studied in long-term ovariectomized (OVX) rats both at the end of a 5-day continuous in vivo pretreatment with LRH and 4-days after cessation of such LRH pretreatment. Rats were on day 0 sc implanted with osmotic minipumps which released LRH at the rate of 250 ng/h. Control rats were implanted with a piece of silicone elastomer with the dimensions of a minipump. On days 2 and 4 the rats were injected with either 3 μg EB or with oil. On day 5 part of the rats were decapitated and the in vitro autonomous (i.e. non-LRH-stimulated) and 'supra-maximally' LRHstimulated release of LH and FSH was studied using a perifusion system. From other rats the minipumps were removed on day 5 and perifusion was performed on day 9. On the 5th day of the in vivo LRH pretreatment the pituitary LH/FSH stores were partially depleted; the pituitaries of the EB-treated rats more so than those of the oil-injected rats. EB alone had no significant effect on the content of the pituitary LH- and FSH stores. On day 9, i.e. 4 days after removal of the minipumps, the pituitary LH and FSH contents had increased in both the oil- and the EB injected rats, but had not yet recovered to control values. In rats not subjected to the 5-days pretreatment with LRH EB had a positive effect on the supra-maximally LRH-stimulated secretion of LH and FSH as well as on the non-stimulated secretion of LH. EB had no effect on the non-stimulated secretion of FSH. After 5 days of in vivo pretreatment with LRH only, the in vitro non-stimulated and supra-maximally LRH-stimulated secretion of both LH and FSH were strongly impaired, the effect correlating well with the LRH-induced depletion of the pituitary LH/FSH stores. In such LRH-pretreated rats EB had on day 5 a negative effect on the (already depressed) LRH-stimulated secretion of LH (not on that of FSH). EB had no effect on the non-stimulated LH/FSH secretion. It could be demonstrated that the negative effect of the combined LRH/EB pretreatment was mainly due to the depressing effect of this treatment on the pituitary LH and FSH stores: the effect of oestradiol on the pituitary LRH-responsiveness (release as related to pituitary gonadotrophin content) remained positive. In LRH-pretreated rats, however, this positive effect of EB was smaller than in rats not pretreated with LRH. Four days after removal of the minipumps there was again a positive effect of EB on the LRH-stimulated secretion of LH and FSH as well as on the non-stimulated secretion of LH. The positive effect of EB on the pituitary LRH-responsiveness was as strong as in rats which had not been exposed to exogenous LRH. The non-stimulated secretion of FSH was again not affected by EB. The results demonstrate that the effect of EB on the oestrogen-sensitive components of gonadotrophin secretion consists of two components: an effect on the pituitary LRH-responsiveness proper, and an effect on the pituitary LH/FSH stores. The magnitude of the effect of EB on the LRH-responsiveness is LRH dependent: it is very weak (almost zero) in LRH-pretreated rats, but strong in rats not exposed to LRH as well as in rats of which the LRH-pretreatment was stopped 4 days previously. Similarly, the effect of EB on the pituitary LH and FSH stores is LRH-dependent: in the absence of LRH, EB has no influence on the contents of these stores, but EB can potentiate the depleting effect of LRH on the LH/FSH-stores. Also this effect disappear after cessation of the LRH-pretreatment.


Seizure ◽  
1999 ◽  
Vol 8 (8) ◽  
pp. 490-493 ◽  
Author(s):  
Erik Taubøll ◽  
Jouko I.T. Isojärvi ◽  
Hanne Flinstad Harbo ◽  
Arto J. Pakarinen ◽  
Leif Gjerstad

2000 ◽  
Vol 88 (6) ◽  
pp. 2240-2245 ◽  
Author(s):  
Thomas H. Reynolds ◽  
Joseph T. Brozinick ◽  
Lisa M. Larkin ◽  
Samuel W. Cushman

The purpose of the present study was to examine the effect of detraining on the glucose transport system after short-term swim training (5 days), long-term swim training (5 wk), and treadmill run training (5 wk). Skeletal muscles were isolated from female Wistar rats at 24 or 48 h posttraining. SST produces a 48% increase in GLUT-4 mRNA, a 30% increase in GLUT-4 protein, and a 60% increase in insulin-stimulated glucose transport activity at 24 h posttraining but not at 48 h posttraining. Similar to SST, long-term swim training produces a 60% increase in GLUT-4 mRNA and a 30% increase in GLUT-4 protein content at 24 h posttraining but not at 48 h posttraining. Finally, treadmill run training produces a transient 35% increase in GLUT-4 protein content that is completely reversed at 48 h after the last bout of exercise. These results demonstrate that the increase in GLUT-4 mRNA and GLUT-4 protein occurs during the first week of exercise training and is rapidly lost after training cessation. We believe that the transient enhancement in GLUT-4 protein after exercise training is due to a short GLUT-4 half-life, a process that is primarily regulated by pretranslational mechanisms.


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


1977 ◽  
Vol 232 (5) ◽  
pp. E478 ◽  
Author(s):  
C Onkelinx

The metabolism of chromium(III) was studied in groups of female Wistar rats of various ages (35, 60, and 120 days) after a single intravenous injection of 51CrCl3 in trace amounts. In all the animals, the plasma disappearance curve could be adequately described by a sum of three exponential terms between 0 and 265 h postinjection. A three-compartment mammillary model is proposed that permits the description of Cr(III) metabolism in quantitative terms. The model defines compartment volumes, clearances by exchange, and clearances by excretion. The total excretory clearance is the sum of three components: urinary clearance (fu), fecal clearance (fd), and a residual clearance (fs), corresponding to an apparently irreversible deposition of chromium into long term body reservoirs. The parameters of the model are reported for each age group; when their values are expressed per 100 g of body wt, all the components of the excretory clearance decrease with age. In all cases elimination takes place primarily via the urine and fs accounts for 31-41% of the total excretory clearance. Consistent with the model, 51Cr was found to accumulate with time in several organs such as bone, kidney, spleen, and liver after a single intravenous injection of 51CrCl3.


1971 ◽  
Vol 68 (3) ◽  
pp. 585-596 ◽  
Author(s):  
O. Helmer Serensen ◽  
Inge Hindberg

ABSTRACT The influence of short-term and long-term treatment with gonadal hormones on the response to calcitonin was investigated in the rat. Oestrogen-treatment, short-term as well as long-term, resulted in a reduced responsiveness to calcitonin. Long-term treatment with androgens enhanced the hypocalcaemic effect of calcitonin in castrated rats of either sex, but reduced the effect in intact animals. No sex differences could be registered in the sensitivity to calcitonin, when intact animals were compared according to age, while marked differences were observed, when the animals were compared according to weight. There was a linear decrease in the response to calcitonin with increasing age in rats of both sexes. An intraperitoneal calcium load was followed by an acute rise in the serum calcium levels. The adult animals counteracted the hypercalcaemia more slowly than the young ones. Significant differences also occurred between male and female rats, the rise in the serum calcium concentration being much more pronounced in the latter group. The hypocalcaemic activity of thyroid tissue from rats of both sexes and of various ages showed considerable variations, but no differences correlated to age or sex.


2014 ◽  
Vol 34 (1) ◽  
pp. 63-71 ◽  
Author(s):  
Ozlem Sangun ◽  
Bumin Dundar ◽  
Hakan Darici ◽  
Selcuk Comlekci ◽  
Duygu Kumbul Doguc ◽  
...  

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


2020 ◽  
Vol 21 (6) ◽  
pp. 787-805
Author(s):  
Ulalume Hernández-Arciga ◽  
David Hernández-Álvarez ◽  
Stefanie Paola López-Cervantes ◽  
Norma Edith López-Díazguerrero ◽  
Adriana Alarcón-Aguilar ◽  
...  

Author(s):  
Milica R Prvulovic ◽  
Desanka J Milanovic ◽  
Predrag Z Vujovic ◽  
Milena S Jovic ◽  
Selma D Kanazir ◽  
...  

Abstract The current study aims to determine the potential benefits of calorie restriction (CR), one of the most promising paradigms for life span and healthspan extension, on cognitive performances in female Wistar rats during aging. As a measure of a healthspan, we evaluated the effects of different onset and duration of CR on frailty level. Female Wistar rats were exposed to either ad libitum (AL) or CR (60% of AL daily intake) food intake during aging. Two different CR protocols were used, life-long CR with an early-onset that started at the adult stage (6 months) and 3-month-long CR, started at the middle (15 months) and late-middle (21 months) age, thus defined as a late-onset CR. The effects of CR were evaluated using open-field, Y-maze, and novel object recognition tests. We broadened 2 tools for frailty assessment currently in use for experimental animals, and in alignment with our previous study, we created a physical–cognitive frailty tool that combines both physical and cognitive performances. Our results clearly showed that CR effects are highly dependent on CR duration and onset. While a life-long restriction with an early-onset has been proven as protective and beneficial, short-term restriction introduced at late age significantly worsens an animal’s behavior and frailty. These results complement our previous study conducted in males and contribute to the understanding of sex differences in a response to CR during aging.


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