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B. Varga and G. Folly

Summary. Oestrous and anoestrous mongrel dogs were anaesthetized with chloralose–urethane. In one group, the ovaries were isolated in situ and the effects of a 15-min infusion of PGF-2α or PGE-2 on perfusion pressure were measured. In the other group, heated thermocouples were introduced into the stroma of each ovary to measure the changes of local blood flow in response to PGF-2α and PGE-2 infused into the ovarian bursa for 15 min. Intra-arterial infusion of 25,50,100 or 200ng PGF-2α/kg/min did not affect perfusion pressure; PGE-2 doses of 3·1, 6·2, 12·5 or 25 ng/kg/min caused reductions in proportion to the dose. All doses of PGF-2α (50·0, 100or 200 ng/kg/min) or PGE-2 (25, 50 or 100 ng/kg/min) increased blood flow in the ovarian stroma in proportion to the dose when administered by infusion into the ovarian bursa. There were no differences in the results from oestrous and anoestrous dogs.

It is concluded that PGF-2α changes intraovarian blood distribution without interfering with the total blood flow while PGE-2 increases both the total and local ovarian blood flow.

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The effects of ACTH and dexamethasone on the uterine weight of immature mice treated with HCG or oestradiol-17β were studied. The animals were treated daily for 3 days and wet and dry uterine weights were measured on the 4th day.

Low doses of ACTH (1·25 μg/day) raised the sensitivity of the uterine weight response to threshold doses of HCG (0·05 to 0·1 i.u.). By increasing the doses of ACTH or HCG, the stimulation gradually turned into inhibition. By itself, ACTH was ineffective and it had no influence on the increase in uterine weight induced by oestradiol-17β. Dexamethasone failed to stimulate the effect of HCG.

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B. Varga, Katalin Csiszár and E. Stark

Institute of Experimental Medicine, Hungarian Academy of Sciences, 1450-Budapest, P.O. Box 67, Hungary

Unilateral ovariectomy is followed by compensatory hypertrophy of the contralateral ovary in the rat (Carmichael & Marshall, 1908; Arai, 1920; Slonaker, 1927). This phenomenon is induced by the increased gonadotrophic hormone release resulting from the decrease of the oestrogen level via a negative feedback mechanism (Heller, Heller & Sevringhaus, 1942; Edgren, Parlow, Peterson & Jones, 1965; Johnson, 1966; Peppler & Greenwald, 1970). After hemiovariectomy the contralateral ovary produces the same number of ova as did both ovaries in the control animals (Peppler, 1972). Of the gonadotrophic hormones, LH increases ovarian blood flow and, since ovarian blood flow is known to increase during oestrus (Wurtman, 1964), the present study was to determine whether the elevated gonadotrophic hormone level resulting from hemiovariectomy increased blood flow in the remaining ovary.

Rats of the CFY strain and weighing 170-200 g were

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D Reglodi, S Cseh, B Somoskoi, B D Fulop, E Szentleleky, V Szegeczki, A Kovacs, A Varga, P Kiss, H Hashimoto, A Tamas, A Bardosi, S Manavalan, E Bako, R Zakany and T Juhasz

PACAP is a neuropeptide with diverse functions in various organs, including reproductive system. It is present in the testis in high concentrations, and in addition to the stage-specific expression within the seminiferous tubules, PACAP affects spermatogenesis and the functions of Leydig and Sertoli cells. Mice lacking endogenous PACAP show reduced fertility, but the possibility of abnormalities in spermatogenic signaling has not yet been investigated. Therefore, we performed a detailed morphological analysis of spermatozoa, sperm motility and investigated signaling pathways that play a role during spermatogenesis in knockout mice. No significant alterations were found in testicular morphology or motility of sperm in homozygous and heterozygous PACAP-deficient mice in spite of the moderately increased number of severely damaged sperms. However, we found robust changes in mRNA and/or protein expression of several factors that play an important role in spermatogenesis. Protein kinase A expression was markedly reduced, while downstream phospho-ERK and p38 were elevated in knockout animals. Expression of major transcription factors, such as Sox9 and phospho-Sox9, was decreased, while that of Sox10, as a redundant factor, was increased in PACAP-deficient mice. The reduced phospho-Sox9 expression was partly due to increased expression and activity of phosphatase PP2A in knockout mice. Targets of Sox transcription factors, such as collagen type IV, were reduced in knockout mice. In summary, our results show that lack of PACAP leads to disturbed signaling in spermatogenesis, which could be a factor responsible for reduced fertility in PACAP knockout mice, and further support the role of PACAP in reproduction.