A specific population of gonadotrophs purified from immature female rat pituitary

Science ◽  
1976 ◽  
Vol 194 (4267) ◽  
pp. 848-851 ◽  
Author(s):  
C Denef ◽  
E Hautekeete ◽  
L Rubin
Keyword(s):  
Female Rat ◽  
Immature Female ◽  
Specific Population ◽  
Rat Pituitary

Rat placental hormones: attempts for identification of rat chorionic gonadotrophin and rat placental lactogen by in vivo experiments

1982 ◽  
Vol 99 (2) ◽  
pp. 288-294 ◽  
Author(s):  
Marco Tabarelli ◽  
R. Kofler ◽  
S. Schwarz ◽  
G. Wick
Keyword(s):  
Limit Of Detection ◽  
Chorionic Gonadotrophin ◽  
Placental Lactogen ◽  
Female Rat ◽  
Immature Female ◽  
Pregnant Rats ◽  
In Vivo Experiments ◽  
Rat Pituitary ◽  
Dose Dependent

Abstract. Rat placental extracts (rPE) were investigated in bioassays for their possible content of rat placental lactogen (rPL) and rat chorionic gonadotrophin (rCG). Luteotrophic and lactogenic activity of rPL was assessed by substitution of rats depleted of endogenous prolactin (Prl) by means of bromoergocryptine (BEC) in early pregnancy and the period of lactation, respectively. The abortifacient effect of a single dose of BEC on day 6 of pregnancy was abolished by rPE equivalent to 1 g rat placenta corresponding to 5 IU bovine Prl (NIH-P-B 2). Substitution was necessary until the evening of day 7 indicating that rPL does not take over the function of Prl before day 8. During lactation rPE reversed the lactation inhibiting effect of daily BEC treatment. In this assay rPL activity corresponded to 1.25–2.5 IU bPrl/g placenta. In order to test for the possible existence of rCG the gonadotrophic activity of rPE was assessed in immature female mice. No gonadotrophic activity was found when rPE equivalent to 1 g rat placenta was administered, whereas equivalents of 3 mg human placenta and 12 mg rat pituitary entailed a dose-dependent response. In this system 0.12 IU human chorionic gonadotrophin (hCG), which served as standard, was the minimal dose (MD) resulting in increased uterine weight. In addition rPE was tested in the immature female rat, where the limit of detection was found to be 0.5 IU hCG. Again no gonadotrophic activity was found in rPE. As the effects of rCG might have been restricted to its presumed target, the corpus luteum of pregnancy, rPE was also tested in pregnant rats depleted of endogenous luteinizing hormone (LH) by a single injection of anti-LH antibodies on day 10 of pregnancy. A MDof 0.5 IU hCG, which served as standard, prevented resorption of foetuses in all animals tested. rPE equivalent to 3.5 g rat placenta, rat pregnancy serum of day 18 and placental transplants could not substitute for endogenous LH.

IN-VITRO STUDIES OF THE EFFECTS OF OESTROGEN PRETREATMENT ON THE SENSITIVITY OF THE IMMATURE FEMALE RAT PITUITARY GLAND TO STIMULATION WITH GONADOTROPHIN RELEASING HORMONE

1977 ◽  
Vol 74 (1) ◽  
pp. 11-21 ◽  
Author(s):  
M. WILKINSON ◽  
D. DE ZIEGLER ◽  
DANIELLE CASSARD ◽  
K. B. RUF
Keyword(s):  
Pituitary Gland ◽  
Brain Lesion ◽  
Culture Technique ◽  
Female Rats ◽  
Female Rat ◽  
Immature Female ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Unilateral Brain Lesion

The effects of oestrogen priming on the sensitivity of the anterior pituitary gland to stimulation with gonadotrophin releasing hormone (GnRH) was investigated in immature female rats using a new organ culture technique. Hemipituitary glands obtained from animals primed with a single dose of oestradiol benzoate (OB; 20 μg/100 g body weight) released significantly more LH when pulsed with GnRH (4 nmol/l) than did control hemipituitary glands. This potentiating effect was detectable as early as 5 days after birth. After a second stimulation, LH secretion remained high. These results were compared with those obtained from animals treated to induce increased levels of endogenous oestrogen on day 26 of life. Thus, hemipituitary glands were obtained from animals given two injections of OB, an injection of pregnant mare serum gonadotrophin (PMSG) or a unilateral brain lesion placed in the basal hypothalamus. Pituitary tissue was stimulated as before with a pulse of GnRH. Two injections of OB enhanced the sensitivity to stimulation. Conversely, both PMSG and lesion treatment severely reduced the sensitivity to GnRH, although PMSG-treated and lesioned animals have been used as models for the study of ovulation.

ANTERIOR PITUITARY SENSITIVITY IN IMMATURE FEMALE RATS STIMULATED WITH GONADOTROPHIN RELEASING HORMONE IN VIVO: EFFECT OF PRIMING WITH OESTROGEN, PREGNANT MARE SERUM GONADOTROPHIN OR BRAIN LESION

1977 ◽  
Vol 74 (1) ◽  
pp. 99-109 ◽  
Author(s):  
D. DE ZIEGLER ◽  
M. WILKINSON ◽  
DANIELLE CASSARD ◽  
K. B. RUF
Keyword(s):  
Brain Lesion ◽  
Treated Group ◽  
Female Rats ◽  
Similar Degree ◽  
Female Rat ◽  
Immature Female ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Pregnant Mare Serum Gonadotrophin

An investigation of pituitary sensitivity, assessed in terms of increments in plasma LH and FSH concentrations, to stimulation with one or two injections of gonadotrophin releasing hormone (GnRH) was carried out on 26-day-old immature female rats which had received one of the following priming treatments: 10 μg oestradiol benzoate (OB) as a single injection on day 23 or day 25, or on both days; 10 i.u. pregnant mare serum gonadotrophin (PMSG) on day 24; an electrochemical brain lesion placed in the mediobasal hypothalamus on day 23; control animals received either vehicle alone or a sham lesion. Pituitary sensitivity assessed at 10.00 h on day 26, after one or two injections of GnRH (100 ng/100 g body weight, s.c.), was enhanced to a similar degree in the three groups treated with OB in terms of LH (P < 0-01). The FSH response also increased after OB treatment but was not statistically significant. In contrast, 48 h after the injection of PMSG (i.e. when the rats were in a 'pro-oestrous-like' condition) pituitary sensitivity in terms of both LH and FSH dropped sharply (P < 0·001). In lesioned animals, pituitary sensitivity to one injection of GnRH was unchanged. A second GnRH injection administered after a 60 min interval induced a slightly larger LH response in control animals. In contrast, the ratio of the second response to the first increased in animals treated with PMSG, despite the state of overall decrease in sensitivity, being 4·5:1 in PMSG-treated rats versus 1·4:1 in controls. In a second set of experiments, we investigated the variation of pituitary sensitivity in conjunction with an experimentally induced gonadotrophin surge. In animals treated with OB on day 23 and with 1 mg progesterone at 12·00 h on day 26, pituitary sensitivity was increased at both 14.00 and 17.00 h as compared with that in the day 23 OB-treated group at 10.00 h. The PMSG-treated animals maintained their state of decreased responsiveness at 14.00 h, but exhibited increased pituitary sensitivity at the time of the gonadotrophin surge (17.00 h). These results show that OB increases pituitary sensitivity to GnRH in 26-day-old female rats and that the induction of a gonadotrophin surge further increases this sensitivity. In contrast, PMSG-treated rats displayed a state of decreased responsiveness 48 and 52 h, but not 55 h, after the injection. Pituitary sensitivity on the second day after PMSG treatment thus clearly differs from that observed during pro-oestrus in the adult cyclic female rat.

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