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SUMMARY
In an attempt to interfere pharmacologically with the feedback action of oestrogen in the ferret, clomiphene citrate was given to anoestrous animals for 10 days, and to oestrous females for 7 or 14 days, in doses ranging from 10 μg to 1000 μg daily. With the higher doses oestrogenic effects on the uterus were observed, while arrest of follicular development in the ovaries indicated inhibition of gonadotrophin secretion. Enhancement of gonadotrophin secretion in anoestrous females was not encountered, although ovulation in oestrous females was an occasional consequence of treatment with the drug.
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SUMMARY
The effect of exposure to long-day conditions, begun at different times during the summer and autumn, on the timing of oestrus in the ferret has been studied. When ferrets were transferred to 16 hr. days in July or August, oestrus set in very rapidly or was inhibited, but when ferrets were subjected to prolonged illumination later in the year, in October or November, a more typical response ensued in that the animals came into heat after about 6 weeks.
Loss of hair, which proceeded to the development of bald areas, was observed after long exposure to 16 hr. light daily.
The period of illumination was reduced from 16 to 8 hr. daily for seven animals which had failed to come into heat after extended exposure to long-day conditions. After 8 weeks, long days were re-imposed and oestrus rapidly ensued in six females. Marked growth of hair took place under short-day conditions.
Exposure to short-day conditions from birth was compatible with a normal timing of oestrus in eight out of 12 females.
It is concluded that under certain conditions prolonged illumination can inhibit the secretion of gonadotrophin in the ferret and block the manifestation of an inherent rhythm of sexual activity.
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SUMMARY
The operation of an ovarian feedback mechanism in the control of pituitary function in the ferret has been tested in anoestrous and in oestrous animals by removing one gonad to determine whether compensatory hypertrophy of the remaining organ occurred, and by the administration of gonadal steroids.
Compensatory ovarian hypertrophy was found after 10 days in both anoestrous and oestrous ferrets. Oestradiol or oestradiol benzoate occasionally caused ovulation after injection into oestrous females, and inhibition of follicular development occurred after s.c. implantation of a tablet of oestradiol. Ovulation also took place in two out of three ferrets injected with oestradiol benzoate (100 μg.) together with progesterone (2 mg.); one out of five animals given 2 mg. progesterone alone ovulated.
These experiments show that release of gonadotrophin by the ferret hypophysis can be modified by gonadal steroids.
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The effect of hypophysectomy or of division of the pituitary stalk on the growth and function of the corpora lutea in the ovaries of the pseudopregnant ferret was studied, and compared with the changes seen in the ovaries and uterus of normal animals. Hypophysectomy caused a fall in the weight of the ovaries and uterus and regression of the corpora lutea. Isolation of the pituitary gland from the brain was compatible with full development of the corpora lutea and did not interfere with the growth of the uterus during the first 4 weeks of pseudopregnancy. Later on, the ovarian and uterine weights fell below those of control animals. Blank operations, and stalk section with subsequent regeneration of the portal vessels, did not disturb luteal function. It is concluded that the pituitary gland of the pseudopregnant ferret secretes a luteotrophic hormone and that an additional factor, possibly oestrogen, may be required for optimal luteal activity.
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Ovarian tissue was autografted to the spleen or kidney of spayed anoestrous or oestrous ferrets to see whether inactivation of ovarian hormones occurred in the liver and to examine the feedback action of gonadal hormones on gonadotrophin secretion. Although the grafts survived in both sites as did homografts made in anoestrous females, the secretion of gonadal hormones was sufficient to cause oestrus only in a minority of animals and there was little difference in the function of grafts made to the spleen or kidney. Vulval swelling and uterine growth were caused by pellets of oestradiol inserted into the spleen so that it appears that this steroid can pass through the liver without loss of oestrogenic activity. It is concluded that little inactivation of gonadal steroids by the liver of the ferret takes place.
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The changes in plasma levels of LH and FSH were examined after treatment of intact and ovariectomized female ferrets with a long-acting analogue of gonadotrophin releasing factor (Gn-RF) (d-Ser(But)6-LH-releasing hormone(1–9)-nonapeptide ethylamide; Hoe 766) either as a single intravenous injection or daily for 6 days. The responses were compared with those induced by daily injections of Gn-RF or 0·9% NaCl (w/v). Treatment with Gn-RF consistently induced rises in both LH and FSH release with peak levels of both hormones being reached 20 min after injection and being of similar size from day to day in individual animals. Thereafter, the gonadotrophin levels declined rapidly to approach basal values by the end of each sampling period. Treatment with Hoe 766, however, produced very high values on day 1 of treatment, with LH being raised for 10–12 and FSH for up to 24 h. Subsequent injections, on the other hand, produced an abbreviated LH response of similar size to that induced by Gn-RF and little, if any, FSH response. In ovariectomized ferrets, Hoe 766 induced a variable LH response and little FSH response at any time. In addition, basal FSH levels in the first three samples taken on each day from day 2 onwards tended to decline markedly in all of the Hoe 766-treated animals, an effect not seen in Gn-RF or 0·9% NaCl-treated controls.
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According to Denamur, Martinet & Short (1970), the luteotrophic effect of oestrogen in the sheep could be the result of three distinct physiological processes: (i) an action of the hormone upon the hypothalamus or hypophysis to alter gonadotrophin secretion, (ii) a direct action upon the corpora lutea, or (iii) the modification of uterine activity to inhibit the release of luteolysin, depending upon the amount of hormone given. They favoured the last possibility, although they noted that oestrogen could also be luteolytic, perhaps by hastening the release of luteolysin.
In a previous communication we reported that acute treatment with ovarian steroids on day 13 of the guinea-pig oestrous cycle had no lasting effect on gonadotrophin secretion, as judged by follicular histology, but markedly altered the sizes of the corpora lutea of the previous ovulation in animals killed 2 days later (Donovan & Lockhart, 1972a). While a single injection of 25 μg
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SUMMARY
The growth and functional activity of luteal bodies formed in the ovaries of guinea-pigs given exogenous gonadotrophin was examined. Folliclestimulating hormone, luteinizing hormone, both hormones together, and both hormones supplemented with prolactin, were given on day 13. Vaginal oestrus occurred 8–12 days later, irrespective of the kind of hormone given. The sizes of luteal bodies induced in intact and hysterectomized guinea-pigs were compared with those of similarly aged naturally formed corpora lutea 8 and 11 days after ovulation. The artificially induced bodies were smaller than normal corpora lutea, but grew to match their size after hysterectomy.
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Department of Physiology, Institute of Psychiatry, De Crespigny Park, London, SE5 8AF and * Department of Obstetrics and Gynaecology and WHO Collaborating Centre for Research on Human Reproduction, King's College Hospital Medical School, Denmark Hill, London, S.E.5
(Received 17 August 1977)
In children with gonadal dysgenesis (45, XO), the concentrations of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) are greatly raised during infancy, fall between the ages of 6–10 years to approach the values for normal children and then rise sharply at about the time puberty would have been expected (Penny, Guyda, Baghdassarian, Johanson & Blizzard, 1970; Conte, Grumbach & Kaplan, 1972; Grumbach, Roth, Kaplan & Kelch, 1972; Kelch, Conte, Kaplan & Grumbach, 1972; Job, Garner, Chaussian, Scholler, Toublanc & Calorbe, 1974). The cause of the 'pubertal' rise in gonadotrophin secretion, or of the fall during late infancy, is not known and in order to see whether this effect occurred
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SUMMARY
The response of the guinea-pig corpus luteum to the luteolytic influence of glass beads placed in the uterus, or to prostaglandin administration, was followed by assay of the progesterone content of blood samples collected daily. Following the introduction of glass beads into the uterus early in the cycle, the secretion of progesterone was curtailed. Treatment with prostaglandin F2α over days 4–6 or 6–8 of the cycle temporarily depressed progesterone release without shortening the life of the corpora lutea. When the drug was administered over days 8–10, 10–12 or 12–14 the depression in progesterone was not followed by any recovery.
These observations indicate that the response of the corpora lutea to a luteolytic influence changes during the oestrous cycle.
