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J. RZĄSA and Z. EWY

Summary.

Intravenous injection of vasotocin in the hen induced premature oviposition within a few minutes. The sensitivity of the oviduct both to vasotocin and oxytocin rose towards the time of normal oviposition. Vasotocin exhibited a much greater oviposition-inducing activity than oxytocin.

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J. RZĄSA and Z. EWY

Summary.

In anaesthetized hens, intravenous injections of vasotocin and oxytocin increased the intrauterine pressure. The response to vasotocin was much more intensive than to oxytocin.

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J. NIEZGODA, J. RZĄSA and Z. EWY

Summary.

The vasotocin level in the blood of hens during oviposition was determined on the isolated bladder of the frog, Rana esculenta. It was found that 10 min before oviposition, the vasotocin level in blood suddenly increased. During oviposition, it was forty-six times higher (P<0·01) than that in hens with no egg in the uterus. After oviposition, the activity of vasotocin in the blood rapidly decreased.

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R. J. Etches, J. B. Williams and J. Rzasa

Summary. Ovarian regression was induced in hens by infusing 30 μg corticosterone/h, feeding diets deficient in Ca2+ or Na+ and by withdrawal of food and water. The weight of the ovary was most severely reduced by the corticosterone infusion. The total number of normal ovarian follicles weighing > 0·012 g was not altered by any of the treatments. However, the number of large yolk-filled follicles decreased while the numbers of smaller follicles and atretic follicles increased when ovarian regression was induced by dietary changes or hormone infusion as compared to normally fed or solvent-infused hens.

These experimental treatments resulted in decreases in plasma concentrations of LH, progesterone and oestradiol, and increases in the plasma levels of corticosterone. These changes were immediate except for the low sodium diet with which there was a delay of about 6 days. When fasted birds were fed oats and given water, plasma LH and oestradiol, but not progesterone, increased. The infusion of corticosterone did not affect the ability of the pituitary gland to secrete LH after an injection of LH-RH, but this response was reduced or eliminated by the other experimental treatments. It is concluded that the regression of the ovary induced by these experimental treatments is a consequence of the reduction in the secretion of LH, which may itself be caused by increased plasma levels of corticosterone. It also appears that recruitment of follicles in the maturational stage which precedes entry into the hierarchy of large yolky follicles was unaffected by all of the methods of inducing ovarian regression which were studied.

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HE Paczoska-Eliasiewicz, A Gertler, M Proszkowiec, J Proudman, A Hrabia, A Sechman, M Mika, T Jacek, S Cassy, N Raver and J Rzasa

Thirty-four-week-old laying hens received injections of recombinant chicken leptin to assess the role of leptin in avian ovarian function. In the first experiment, the hens (n=60) were divided into three groups: (i). fed ad libitum; (ii). fasted; and (iii). fasted + leptin. Hens were fasted for 5 days and those treated with leptin received 250 microg leptin kg-1 body weight twice a day, i.p. In the second experiment, the hens (n=72) were divided into four groups: (i). fed ad libitum; (ii). fasted; (iii). fasted + leptin given only during fasting (5 days); or (iv). fasted and leptin given during both fasting and 5 days of re-feeding (10 days). LH was measured in blood plasma, and progesterone and oestradiol were measured in blood plasma and the ovary by radioimmunoassay. Apoptosis was examined in the walls of the three largest yellow hierarchical follicles (F3-F1; F3 25-35 mm) by the TdT-mediated dUTP nick-end labelling method. Results showed that the injections of leptin during fasting: (i). delayed cessation of egg laying; (ii). attenuated regression of yellow hierarchical follicles; (iii). altered ovarian steroidogenesis; and (iv). abolished the fasting-induced apoptosis in the wall of F3-F1 follicles during the first 2 days of fasting and partially attenuated apoptosis after 5 days of fasting. Prolongation of leptin injections into the re-feeding period considerably delayed the restoration of the ovary. Expression of leptin receptor in laying hens was determined by RT-PCR. The highest expression of leptin receptor was observed in the hypothalamus. Lower receptor mRNA expression was found in the hypophysis, whereas the lowest expression was observed in the ovary. Within the ovary, a relatively high expression of leptin receptor was found in the stroma with cortical follicles <1 mm, the wall of white (1-8 mm) and small yellow follicles (>8-12 mm), and the granulosa layer of F3 follicles. The expression of leptin receptor in the granulosa layer of F2 and F1 follicles was barely detectable. This was in contrast to a much higher expression of leptin receptor maintained in the theca layer of F3-F1 follicles. The present results indicate that in chickens leptin might be involved in the adaptation to starvation due to attenuation of follicular apoptosis. The presence of leptin receptors in the ovary indicates the possibility of a peripheral effect of the hormone.