Structural luteolysis in hypophysectomized rats

Malven, P.V.; Cousar, GJ; Row, EH

doi:10.1152/ajplegacy.1969.216.2.421

Cited by 11 publications

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“…In unpublished experiments with rats in which "superovulation" was induced by administration of 50 IU PMS foUowed by 25 IU HCG, hypophysectomy has been observed to decrease mean ovarian weights (both ovaries) to 144 + 5 mg, from the level of 174 + 5 mg observed in intact rats at the same stage of development. Prolactin therapy, at the same dosage as used in the present experiments, failed to restore ovarian weight (144 + 5 mg) in hypophysectomized rats, whereas growth hormone (200 ng twice daily), which restored body growth to 88% of intact controls, resulted in mean ovarian weights of 192 + 4 mg. A similar effect of growth hormone on weights of luteinized ovaries of hypophysectomized rats has been reported recently by Malven et al (12).…”

Section: Discussionsupporting

confidence: 86%

Effects of Prolactin Upon Cholesterol Metabolism and Progesterone Biosynthesis in Corpora Lutea of Rats Hypophysectomized During Pseudopregnancy¹

1970

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The effects of hypophysectomy and of replacement therapy with prolactin upon in vitro biosynthesis of progesterone and 20a-hydroxypregn-4-en-3-one and of several lipid constituents in isolated corpora lutea of pseudopregnant rats have been investigated. Pseudopregnancy was induced by mechanical stimulation of the uterine cervices of rats in which first estrus and ovulation were synchronized by sc administration of 4 IU pregnant mare serum gonadotropin (PMS) at 30 days of age. Hypophysectomy, performed on the second day after ovulation, resulted in marked inhibition of net in vitro synthesis of progesterone in corpora lutea obtained at autopsy 5 days later. In contrast, in vitro synthesis of 20a-hydroxypregn-4-en-3-one was markedly stimulated by this treatment, with the result that "total progestin" (progesterone plus 20a-hydroxypregn-4-en-3-one) synthesis was not significantly altered. Prolactin treatment (200 M g NIH-P-S6, twice daily) completely prevented these changes, actually increasing the level of progesterone synthesis above that of the intact, pseudopregnant controls, as well as decreasing the level of synthesis of 20«-hydroxypregn-4-en-3-one below that of the same control animals. Under the same experimental conditions, estradiol administration effectively induced cornification of vaginal mucosae and distention of uteri with fluid only in those rats which were hypophysectomized but received no prolactin; prolactin administration abolished both these responses, confirming the ability of this hormone to induce secretion of progesterone in "progestational" amounts. No effect of estradiol itself upon synthesis of either steroid, either in the absence or presence of prolactin, was observed. Levels of cholesterol (both free and esterified) in corpora lutea were not altered significantly as a result of hypophysectomy, but prolactin treatment increased concentration of both forms of this lipid. In vitro incorporation of acetate-l-u C in both free cholesterol and esterified sterols was decreased as a result of hypophysectomy. Prolactin therapy resulted in only slight increases in acetate-l-14 C incorporation into these compounds in the absence of the pituitary, in marked contrast to the previously observed ability of this hormone to effect approximately 10-fold increases in synthesis of these compounds in intact rats. Incorporation of acetate-l-14 C into longchain fatty acids of 4 classes of lipids (sterol esters, triglycerides, phospholipids and free fatty acids) was not significantly altered by hypophysectomy, but was markedly augmented by prolactin treatment. (Endocrinology 86: 634, 1970)

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Section: Discussionsupporting

confidence: 86%

Effects of Prolactin Upon Cholesterol Metabolism and Progesterone Biosynthesis in Corpora Lutea of Rats Hypophysectomized During Pseudopregnancy¹

1970

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“…The preovulatory PRL surge on the evening of proestrus induces luteolysis in either the CL of the current or previous cycles [2]. Structural luteolysis can be also induced in hypophysectomized [7][8][9][10][11] or cycling [2,4,6] 1 This work has been subsidized by grants 1FD97-1065-CO3-03 and PM98-0167 from the Direcció n General de Enseñ anza Superior e Investigació n Cientifica, Spain. rats by exogenous PRL administration.…”

Section: Introductionmentioning

confidence: 99%

Luteolytic Effect of Prolactin Is Dependent on the Degree of Differentiation of Luteal Cells in the Rat1

Gaytán¹,

Bellido²,

Morales³

et al. 2001

Biology of Reproduction

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We studied the morphological and quantitative changes in cyclic corpora lutea (CCL) and in CL of pregnancy (CLP) during structural luteolysis. Elimination of CCL takes several cycles, and cell death occurs as successive apoptotic bursts, from 2100 h in proestrus to 1300 h in estrus. Each apoptotic burst determined a 60% decrease in the CL volume and an 80% decrease in the number of steroidogenic cells (SC). All these changes were inhibited by blocking the preovulatory prolactin (PRL) surge with bromocryptine (CB154). Neither apoptotic cells nor changes in the number of SC were found in regressing CLP from Day 21 of pregnancy to Day 2 postpartum, although there was a 50% decrease in the CLP volume and a 30% decrease in the mean cross-sectional area of SC. Treatment with CB154 on the day of parturition did not modify these regressive changes. On Day 5 postpartum, the volume of the CLP and the number of SC were equivalent in lactating rats (showing high PRL concentrations induced by pup suckling) and nonlactating noncycling rats (in which cyclicity and, therefore PRL surges, were blocked by treatment with LHRH antagonist). However, on Day 10 postpartum, the CLP volume and the number of SC were significantly decreased in lactating rats, and apoptotic cells were frequent. In postpartum cycling rats, the CLP did not show apoptotic cells on the day of the second postpartum estrus (on Day 5 postpartum), whereas on the day of the third postpartum estrus (on Day 9 postpartum), apoptotic cells were abundant. These results indicate that PRL does not induce apoptosis in the CLP before Day 5 postpartum and strongly suggest that the proapoptotic effect of PRL is dependent on the degree of differentiation of luteal cells.

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“…In the cyclic rat, prolactin (PRL) is very important for structural luteal regression. In hypophysectomized rats, structural regression is restrained, and the luteal structure remains in the ovary for several months [7]. On the other hand, in the hypophysectomized cyclic hamster, the CL regresses at the same time as in intact cyclic animals [8].…”

mentioning

confidence: 99%

The Effects of Prolactin and Gonadotropin on Luteal Function and Morphology in the Cyclic Golden Hamster

Kon

Kishi

Arai

et al. 2008

Journal of Reproduction and Development

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Abstract. The present study was conducted to evaluate the endocrinological effects of the pituitary on luteal maintenance and regression in the cyclic golden hamster (Mesocritus auratus). After hypophysectomy (Hypox) at 0900 h on day 1 of the estrous cycle (the day of ovulation), the animals received injection of prolactin (PRL) or PRL plus equine chorionic gonadotropin (eCG). They were decapitated at 1500 h on day 3 of the cycle, and trunk blood was collected for measurement of progesterone (P4). Corpora lutea (CLs) were dissected from one ovary for DNA ladder detection by electrophoresis, determination of DNA fragmentation ratio by fluorometric measurement method and measurement of P4. The other ovary was used for histological observation. After the Hypox, the daily injection of 1 mg ovine PRL restrained the DNA fragmentation ratio and number of apoptotic cell in the CLs. The PRL treatment maintained the luteal morphology and increased the luteal P4 concentration, but not in the plasma P4 concentration. In addition to PRL, injection of 2 IU eCG after the Hypox also restrained the DNA fragmentation ratio and number of apoptotic cells in the CLs to the level of a pregnant animal. The PRL plus eCG treatment maintained the luteal morphology in the same manner as the PRL only treatment and increased not only the luteal but also the plasma P4 concentration. These results suggest that PRL restrains luteal apoptosis and maintains luteal morphology and that the combination of PRL and eCG restrains not only structural but also functional luteal regression in the cyclic hamster. Key words: Apoptosis, Corpus luteum, Golden hamster (Mesocritus auratus), Hypophysectomy, Prolactin (PRL) (J. Reprod. Dev. 54: [418][419][420][421][422][423] 2008) he corpus luteum (CL) is a transient endocrine organ required for normal pregnancy in mammals. The most important function of the CL is to secrete progesterone (P4). If pregnancy does not occur, the CL must regress to allow initiation of a new reproductive cycle. Luteal function and structure are regulated by luteotropic and luteolytic hormones. Luteotropic hormones maintain and activate the CL, and luteolytic hormones lead the CL to regression. Whereas the factors regulating follicle development, ovulation and luteinization are common to many mammalian species, the luteotropic and luteolytic factors are different between species [1-3].The estrous cycle of the golden hamster lasts exactly 4 days (day 1=ovulation day), and the functional life span of the CL is limited to the first 2 days of the cycle. Serum P4 levels decrease drastically at the end of day 2 (functional luteal regression) [4]. Following functional regression, the CL shows signs of structural regression on day 3 of the cycle and vanishes by the next ovulation [5,6]. This rapidity of structural regression is a feature of hamster luteolysis. In the rat, although the functional life span of the CL is about 2 days as in the hamster, the luteal structure persists for 3-4 cycles [1,3]. This difference suggests that the regul...

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Structural luteolysis in hypophysectomized rats

Cited by 11 publications

References 0 publications

Effects of Prolactin Upon Cholesterol Metabolism and Progesterone Biosynthesis in Corpora Lutea of Rats Hypophysectomized During Pseudopregnancy¹

Effects of Prolactin Upon Cholesterol Metabolism and Progesterone Biosynthesis in Corpora Lutea of Rats Hypophysectomized During Pseudopregnancy¹

Luteolytic Effect of Prolactin Is Dependent on the Degree of Differentiation of Luteal Cells in the Rat1

The Effects of Prolactin and Gonadotropin on Luteal Function and Morphology in the Cyclic Golden Hamster

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Structural luteolysis in hypophysectomized rats

Cited by 11 publications

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Effects of Prolactin Upon Cholesterol Metabolism and Progesterone Biosynthesis in Corpora Lutea of Rats Hypophysectomized During Pseudopregnancy1

Effects of Prolactin Upon Cholesterol Metabolism and Progesterone Biosynthesis in Corpora Lutea of Rats Hypophysectomized During Pseudopregnancy1

Luteolytic Effect of Prolactin Is Dependent on the Degree of Differentiation of Luteal Cells in the Rat1

The Effects of Prolactin and Gonadotropin on Luteal Function and Morphology in the Cyclic Golden Hamster

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Effects of Prolactin Upon Cholesterol Metabolism and Progesterone Biosynthesis in Corpora Lutea of Rats Hypophysectomized During Pseudopregnancy¹

Effects of Prolactin Upon Cholesterol Metabolism and Progesterone Biosynthesis in Corpora Lutea of Rats Hypophysectomized During Pseudopregnancy¹