SITE OF MODULATORY ACTION OF OESTROGEN AND PROGESTERONE ON GONADOTROPHIN RESPONSE TO LUTEINIZING HORMONE RELEASING FACTOR

1977 ◽  
Vol 73 (1) ◽  
pp. 165-170 ◽  
Author(s):  
G. FINK ◽  
S. R. HENDERSON
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Female Rats ◽  
Pituitary Stalk ◽  
Spontaneous Release ◽  
Medial Basal Hypothalamus ◽  
Hypothalamic Deafferentation ◽  
Full Effect ◽  
The Brain

SUMMARY The effect of oestrogen and progesterone on the spontaneous release of gonadotrophins and on the gonadotrophin response to luteinizing hormone releasing factor has been examined in female rats subjected to hypothalamic deafferentation or pituitary stalk section. The results indicate that both steroids act at the level of the medial basal hypothalamus as well as the anterior pituitary gland; progesterone, for its full effect, also requires the integrity of connexions of the hypothalamus with other areas of the brain.

Prostaglandin D2 induces release of luteinizing hormone from the rat pituitary gland without the modulation of hypothalamic luteinizing hormone releasing hormone

1983 ◽  
Vol 99 (2) ◽  
pp. 289-292 ◽  
Author(s):  
K. Tasaka ◽  
A. Miyake ◽  
T. Sakumoto ◽  
T. Aono ◽  
K. Kurachi
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Direct Action ◽  
Female Rats ◽  
Prostaglandin D2 ◽  
Medial Basal Hypothalamus ◽  
Releasing Hormone ◽  
In Series ◽  
Lh Release ◽  
Lh Releasing Hormone

The effect of prostaglandin D2 (PGD2) on release of LH and LH releasing hormone (LHRH) was studied in a sequential double-chamber superfusion system using the medial basal hypothalamus (MBH) and the pituitary gland from female rats at dioestrus. Infusion of PGD2 (5·7 or 57μmol/l) caused a significant (P <0·05) increase in LH release to values 40–60% above the preinjection values from the pituitary gland superfused either alone or in series with the MBH. No release of LHRH in response to PGD2 was observed from the superfused MBH. These data demonstrate that PGD2 causes LH release from the pituitary gland not by inducing release of hypothalamic LHRH but by a direct action on the gland.

OVARIAN STEROID EFFECTS ON GONADOTROPHIN OUTPUT, AND ON THE INCORPORATION OF 35S FROM METHIONINE INTO PROTEIN OF DISCRETE BRAIN AREAS AND THE ANTERIOR PITUITARY

1977 ◽  
Vol 85 (2) ◽  
pp. 279-290
Author(s):  
M. B. ter Haar ◽  
P. C. B. MacKinnon
Keyword(s):  
Luteinizing Hormone ◽  
Median Eminence ◽  
Anterior Pituitary ◽  
Preoptic Area ◽  
Ovarian Hormones ◽  
Female Rats ◽  
Brain Areas ◽  
Lh Surge ◽  
Progesterone Metabolites ◽  
The Brain

ABSTRACT The effects of various ovarian hormones administered on the morning of pro-oestrus on gonadotrophin levels and the incorporation of 35S from methionine into protein of discrete areas of the brain and the anterior pituitary were investigated at 15.00 h of the same day in female rats. The hormones which were investigated in this study could be divided in general into two groups according to their actions. The first group, consisting of oestradiol-17β and progesterone, tended to advance the preovulatory surge of luteinizing hormone (LH) by 3–6 h from 18.00–21.00 h, together with the peaks of [35S] incorporation in the median eminence area and the anterior pituitary which normally accompany the LH surge. The second group, consisting of the LH-stimulated reduced progesterone metabolites, 5α-pregnane-3,20-dione (pregnanedione) and 20α-hydroxypregn-4-en-3-one (dihydroprogesterone), tended to inhibit serum gonadotrophin levels as well as inhibiting the pro-oestrous increase of [35S] incorporation in the median eminence area and in the amygdala, but not in the preoptic area and the anterior pituitary. On the afternoon of pro-oestrus in intact animals, luteinizing hormonereleasing hormone or LH administration had the same effect on [35S]incorporation in the brain as did the progesterone metabolites, though this effect was not observed if the animals had been ovariectomized a few hours beforehand. It is suggested that certain ovarian hormones are involved in the neural events which induce the pre-ovulatory LH surge, while others are associated with neural events which terminate the stimulus for the LH surge.

EFFECT OF INTRAVENOUS INFUSION OF A STEROID ANAESTHETIC ON THE PREOVULATORY SURGE OF LUTEINIZING HORMONE AND OVULATION IN INTACT RATS

1978 ◽  
Vol 76 (2) ◽  
pp. 361-362 ◽  
Author(s):  
J. RABII ◽  
D. K. CLIFTON ◽  
C. H. SAWYER
Keyword(s):  
Los Angeles ◽  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Critical Period ◽  
Brain Research ◽  
Anterior Pituitary Gland ◽  
Female Rats ◽  
School Of Medicine ◽  
Intact Rats

Department of Anatomy and Brain Research Institute, UCLA School of Medicine, Los Angeles, California 90024, U.S.A. (Received 21 July 1977) The existence of a 'critical period' in the ovulatory surge of pituitary gonadotrophin during the afternoon of pro-oestrus was demonstrated by Everett, Sawyer & Markee (1949). It was assumed that during this period, between 14.00 and 16.00 h, an amount of gonadotrophin sufficient to cause ovulation was released from the anterior pituitary gland. Administration of a number of neuropharmacologically active drugs before or during the 'critical period' was shown to inhibit the ovulatory response (Everett, 1961). Recently, Blake (1974) described the existence of an 'activation period' as well as a 'potential activation period' for the preovulatory release of luteinizing hormone (LH) in female rats. The 'activation period' is an extended 'critical period', from 14.00 to 17.00 h, during which time a neurohumoral signal continues to stimulate the anterior pituitary gland

ONTOGENY OF THE SENSITIZING EFFECT OF OESTRADIOL AND LUTEINIZING HORMONE RELEASING HORMONE ON THE ANTERIOR PITUITARY GLAND OF THE FEMALE RAT

1981 ◽  
Vol 91 (2) ◽  
pp. 347-351 ◽  
Author(s):  
R. MEIDAN ◽  
G. FINK ◽  
Y. KOCH
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Priming Effect ◽  
Anterior Pituitary Gland ◽  
Female Rats ◽  
Facilitatory Effect ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh

The ontogeny of the facilitatory effect of oestradiol and luteinizing hormone releasing hormone (LH-RH) on the responsiveness of the anterior pituitary gland to LH-RH has been studied in vitro using pituitary glands from female rats aged 15, 17, 20, 31, 35 and 38 days. The facilitatory effect of oestradiol was already well established by day 15, while the facilitatory effect of LH-RH (priming effect) developed only after day 17. Although it increased the overall response of the gland to LH-RH, oestradiol did not selectively enhance the priming effect of LH-RH. Both the effect of oestradiol and LH-RH reached a peak on day 25, 7 days before vaginal opening in this colony, and, as assessed by measuring pituitary LH contents, were not dependent upon the synthesis of LH. These data show that different mechanisms may be involved in the facilitation of pituitary responsiveness by oestradiol and LH-RH, but that both mechanisms appear to depend more upon an increase in the sensitivity of the receptor/release apparatus rather than in the gonadotrophin content of the gonadotrophs.

OESTRADIOL-17β INCREASES PITUITARY RESPONSIVENESS BY A MECHANISM THAT INVOLVES THE RELEASE AND THE PRIMING EFFECT OF LUTEINIZING HORMONE RELEASING FACTOR

1981 ◽  
Vol 88 (2) ◽  
pp. 301-308 ◽  
Author(s):  
ALISON SPEIGHT ◽  
RACHEL POPKIN ◽  
A. G. WATTS ◽  
G. FINK
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Priming Effect ◽  
Anterior Pituitary Gland ◽  
Silicone Elastomer ◽  
Pituitary Stalk ◽  
Adult Rats ◽  
Peripheral Plasma

We have investigated the mechanism by which oestradiol-17β augments pituitary responsiveness to luteinizing hormone releasing factor (LH-RF). Adult rats were ovariectomized on the morning of dioestrus and implanted with either an empty silicone elastomer capsule or a capsule containing oestradiol-17β. Twelve hours later the LH response, tested by injecting 50 ng LH-RF/100 g i.v., was significantly greater in animals implanted with an oestradiol capsule compared with that in animals implanted with an empty capsule. The effect of oestradiol was blocked by sodium pentobarbitone administered 4 h before the test, and this block was overcome by infusing LH-RF during the 4 h period at doses which by themselves were not sufficient to evoke a large release of LH. We also measured LH-RF in pituitary stalk blood collected under Althesin anaesthesia between 4–6 and 12–13 h after ovariectomy and capsule implantation. The concentration of LH-RF in stalk plasma fell between these two collection periods in animals implanted with empty but not with oestradiol-filled capsules. The concentrations of LH-RF in stalk plasma, although relatively low, were significantly higher in animals bearing an oestradiol-containing capsule than the concentrations in peripheral plasma from similarly treated animals, and, by comparison with the LH-RF concentrations in peripheral plasma from animals infused with LH-RF, were sufficiently high to increase significantly the responsiveness of the pituitary gland. These data show that as well as acting directly on the pituitary gonadotrophs, oestradiol-17β increases the responsiveness of the anterior pituitary gland by a mechanism that involves the release and the priming effect of LH-RF.

Further studies on the regulation, localization and function of the TRH-like peptide pyroglutamyl-glutamyl-prolineamide in the rat anterior pituitary gland

1995 ◽  
Vol 146 (2) ◽  
pp. 293-300 ◽  
Author(s):  
J M M Rondeel ◽  
W Klootwijk ◽  
E Linkels ◽  
P H M Jeucken, W ◽  
L J Hofland ◽  
...  
Keyword(s):  
Body Weight ◽  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland ◽  
Female Rats ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Lhrh Antagonist

Abstract Recent evidence shows that thyrotrophin-releasing hormone (TRH) immunoreactivity in the rat anterior pituitary gland is accounted for by the TRH-like tripeptide prolineamide-glutamyl-prolineamide (pGlu-Glu-ProNH2, <EEP-NH2). The present study was undertaken to investigate further the regulation, localization and possible intrapituitary function of <EEP-NH2. Anterior pituitary levels of <EEP-NH2 were determined between days 5 and 35 of life, during the oestrous cycle and after treatment with the luteinizing hormone-releasing hormone (LHRH) antagonist Org 30276. Treatment of adult males with the LHRH antagonist either for 1 day (500 μg/100 g body weight) or for 5 days (50 μg/100 g body weight) reduced anterior pituitary <EEP-NH2 levels by 25–30% (P<0·05 versus saline-treated controls). Anterior pituitary <EEP-NH2 increased between days 5 and 35 of life. In females, these levels were 2- to 3-fold higher (P<0·05) than in males between days 15 and 25 after birth; these changes corresponded with the higher plasma follicle-stimulating hormone (FSH) levels in the female rats. After day 25, <EEP-NH2 levels in female rats decreased in parallel with a decrease in plasma FSH. Injections with the LHRH antagonist (500 μg/100 g body weight), starting on day 22 of life, led to reduced contents of <EEP-NH2 in the anterior pituitary gland of female rats on days 26 and 30 (55 and 35% decrease respectively). Levels of <EEP-NH2 in the anterior pituitary gland did not change significantly during the oestrous cycle. Fractionation of anterior pituitary cells by unit gravity sedimentation was found to be compatible with the localization of <EEP-NH2 in gonadotrophs. In vitro, <EEP-NH2 dose-dependently inhibited TRH-stimulated growth hormone (GH) release from anterior pituitary cells obtained from neonatal rats, but no consistent effects were seen on the in vitro release of luteinizing hormone (LH), FSH, prolactin (PRL) or thyroid-stimulating hormone (TSH) under basal or TRH/LHRH-stimulated conditions. Furthermore, <EEP-NH2 did not affect the in vitro hormone release by anterior pituitary cells obtained from adult rats. In vivo, <EEP-NH2 (0·3–1·0 μg intravenously) did not affect plasma PRL, TSH, LH, FSH and GH in adult male rats. We conclude that <EEP-NH2 in the anterior pituitary gland is regulated by LHRH, is probably localized in gonadotrophs and may play a (paracrine) role in neonatal GH release. Journal of Endocrinology (1995) 146, 293–300

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