Involvement of norepinephrine in pituitary LH release induced by oestradiol in vitro

1984 ◽  
Vol 107 (2) ◽  
pp. 199-203
Author(s):  
A. Miyake ◽  
K. Tasaka ◽  
T. Aono
Keyword(s):  
Oestrous Cycle ◽  
Female Rats ◽  
Direct Effects ◽  
Significant Release ◽  
Lh Release ◽  
Lh Secretion ◽  
Perifusion System ◽  
Double Chamber

Abstract. The direct effects of oestradiol-17β (E2) on pituitary luteinizing hormone (LH) release and the role of norepinephrine (NE) in E2-induced gonadtrophin release were examined in a sequential double chamber perifusion system by perifusing the mediobasal hypothalami (MBH) and/or pituitaries excised from normally cycling female rats. Administration of E2 induced significant release (70–160% increase, P < 0.05) of LH from the pituitary of rats in pro-oestrus, but not in other stages of the oestrous cycle. When the MBH and the pituitary were perifused in sequence, E2 induced significant release of LH in all stages of the oestrous cycle except oestrus. When the pituitary from rats in dioestrus II was perifused alone with medium containing 200 ng/ml NE, significant release of LH (80–170% increase, P < 0.05) was observed after the administration of E2. The E2-induced LH release in pro-oestrus was completely abolished by perifusion with medium containing diethyldithiocarbamate, an inhibitor of NE synthesis. These findings suggest that NE may be involved in changes of pituitary responsiveness in LH secretion to oestrogen during the rat oestrous cycle.

Vasoactive intestinal peptide stimulates gonadotropin-releasing hormone release from rat hypothalamus in vitro

1988 ◽  
Vol 117 (3) ◽  
pp. 399-402 ◽  
Author(s):  
Shirou Ohtsuka ◽  
Akira Miyake ◽  
Takamichi Nishizaki ◽  
Keiichi Tasaka ◽  
Osamu Tanizawa
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Normal Female ◽  
Gnrh Release ◽  
In Series ◽  
Significant Release ◽  
Lh Release ◽  
Perifusion System

Abstract. The effects of vasoactive intestinal peptide (VIP) on the releases of LH and GnRH were examined in a sequential double chamber perifusion system by perifusing the medio-basal hypothalamus and/or pituitary excised from normal female rats in diestrus or ovariectomized rats. When the medio-basal hypothalamus and pituitary from normal rats in series were perifused with VIP (10−6 mol/l), the concentration of LH in the efflux was increased by 59–181% above that before the injection (P < 0.05), VIP having a dosedependent effect. VIP had no effect on LH release from the pituitary perifused alone. Infusion of VIP at 10−6 mol/l induced a significant release (84–159% increase, P < 0.05) of GnRH from the medio-basal hypothalamus. Infusion of 10−6 mol/l VIP induced a significant release (41–99% increase, P < 0.05) of LH in ovariectomized rats. These findings suggest that VIP induces GnRH release from the medio-basal hypothalamus, resulting in LH release from the pituitary, and that this process does not require ovarian estrogen.

Effect of acute immunoneutralization of endogenous leptin on prolactin and LH secretion during the afternoon of pro-oestrus or in steroid-treated ovariectomized female rats

Reproduction ◽  
2000 ◽  
pp. 39-45 ◽  
Author(s):  
LC Gonzalez ◽  
L Pinilla ◽  
M Tena-Sempere ◽  
C Dieguez ◽  
FF Casanueva ◽  
...  
Keyword(s):  
Prolactin Secretion ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Blood Samples ◽  
Lh Release ◽  
Lh Secretion

Recent data indicate that leptin is involved in the control of reproductive function. Experiments were carried out to analyse the role of endogenous leptin in the regulation of LH and prolactin secretion during the afternoon of pro-oestrus and that induced by ovarian steroids in ovariectomized rats. In the first experiment, cyclic female rats were implanted with intra-auricular and intracerebroventricular (i.c.v.) cannulae and, at pro-oestrus, were injected (i.c.v.) with 10 microliters normal rabbit serum or leptin antiserum (at 13:00 and 14:00 h). Blood samples were obtained at 10:00 h and at intervals of 1 h between 13:00 and 20:00 h. In the second experiment, female rats in pro-oestrus were injected with normal rabbit serum or leptin antiserum at 16:00 and 18:00 h and blood samples were taken every 10 min between 18:00 and 20:00 h. In the third experiment, adult female rats that had been ovariectomized 2 weeks before were implanted with intra-auricular and i.c.v. cannulae and treated with oestradiol benzoate (30 micrograms s.c.) at 10:00 h and progesterone (2 mg s.c.) 48 h later. Normal rabbit serum (10 microliters) or leptin antiserum (10 microliters) were injected (i.c.v.) at 13:00 and 14:00 h, and blood samples were obtained at 10:00 h and at intervals of 1 h between 13:00 and 20:00 h. In the fourth experiment, hemipituitaries from ovariectomized steroid-treated female rats were incubated in the presence of leptin116-130 (an active fragment of the native molecule), GnRH or leptin + GnRH. Prolactin and LH secretion during the afternoon of pro-oestrus in females treated with leptin antiserum was similar to that observed in animals injected with normal rabbit serum. In ovariectomized female rats, the steroid-induced LH surge increased slightly after administration of leptin antiserum, whereas the prolactin surge remained unchanged. In vitro, leptin116-130 (10(-5) to 10(-8) mol l-1) inhibited LH secretion and modulated the effect of GnRH on LH release, depending on the concentration of GnRH: leptin116-130 (10(-6) mol l-1) reduced the effectiveness of 10(-7) mol GnRH l-1 and increased that of 10(-9) mol GnRH l-1. In conclusion, these experiments indicate that acute immunoneutralization of endogenous leptin does not interfere with spontaneous or steroid-induced LH and prolactin surges. In addition, the finding that leptin116-130 inhibited LH release and modulated the effectiveness of GnRH in vitro provides evidence of the direct modulatory role of leptin on LH secretion acting at the pituitary.

Oxytocin modulates the luteinizing hormone response of the rat anterior pituitary to gonadotrophin-releasing hormone in vitro

1995 ◽  
Vol 145 (1) ◽  
pp. 113-119 ◽  
Author(s):  
J J Evans ◽  
S J Hurd ◽  
D R Mason
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
The Self ◽  
Female Rats ◽  
Hormone Response ◽  
Priming Process ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion

Abstract Although GnRH is believed to be the primary secretagogue for LH, oxytocin has also been shown to stimulate LH release from the anterior pituitary. We investigated the possibility that the two secretagogues interact in the modulation of LH release. Anterior pituitaries were removed from adult female rats at pro-oestrus, and tissue pieces were pre-incubated in oxytocin for 3 h prior to being stimulated with 15 min pulses of GnRH. LH output over the 1 h period from the beginning of the GnRH pulse was determined. Control incubations were carried out in the absence of oxytocin, and background secretory activities without GnRH stimulation were also determined. Tissue which was pre-exposed to oxytocin (0·012–1·25 μm) had an increased LH response to GnRH (1·25 nm). The increase was larger than the sum of the LH outputs obtained with oxytocin and GnRH separately, revealing that oxytocin synergistically enhanced LH secretion elicited by GnRH (P<0·05; ANOVA). If stimulation by GnRH was delayed for 2 h after incubation with oxytocin, an increase in LH secretion was still observed, indicating that oxytocin-induced modulation did not rapidly disappear. Oxytocin pre-incubation was observed to result in an increase of maximal GnRH-induced LH output (P<0·001; t-test), as well as an increase of intermediate responses. The LH response of the anterior pituitary to subsequent pulses of GnRH was modified by the self-priming process. The effect of oxytocin pretreatment on the response of primed tissue to GnRH was also investigated. It was found that pre-incubation in oxytocin also enhanced the LH response of primed tissue to GnRH. The study has revealed that oxytocin increases the LH output of anterior pituitary tissue in response to GnRH. The effect occurs on both GnRH-primed and unprimed tissues. The results suggest that oxytocin has the potential to regulate the dynamics of the pro-oestrous LH surge. Journal of Endocrinology (1995) 145, 113–119

Suppressive effect of prolactin on oestrogen-induced secretion of LH by sequentially perifused rat hypothalamus-pituitary

1985 ◽  
Vol 108 (2) ◽  
pp. 151-155 ◽  
Author(s):  
Jin-Woo Lee ◽  
Akira Miyake ◽  
Keiichi Tasaka ◽  
Shirou Otsuka ◽  
Toshihiro Aono ◽  
...  
Keyword(s):  
Experimental Period ◽  
Suppressive Effect ◽  
Control Group ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
Lh Secretion ◽  
Hypothalamic Level ◽  
Experimental Group ◽  
Perifusion System

Abstract. The effect of prolactin (Prl) on oestrogeninduced gonadotrophin secretion was examined in vitro in a sequential double chamber perifusion system. As control groups, mediobasal hypothalamus (MBH)-pituitary pairs or pituitaries without the MBHs were perifused with Medium 199. As an experimental group, MBH-pituitary pairs were perifused with Medium 199 containing 1 μg/ml of rat Prl. These groups were stimulated with 10−7m oestradiol-17β (E2) for 30 min, and luteinizing hormone (LH) in the serial fractions of effluent was measured. In the control group of MBH-pituitary pairs perifused with medium without Prl, secretion of LH began to rise within 30 min after the beginning of stimulation, reached a peak 30 min after the end of stimulation and then remained at a plateau for the rest of the experimental period, whereas in the control group of pituitaries alone no significant response was observed. In the experimental group perifused with medium containing Prl, LH-secretion showed peaks 20 and 80 min after the end of E2-stimulation, respectively, and the first peak was significantly (P < 0.01) less than the level in the control group. These data demonstrate that Prl at this concentration suppressed the rapid LH release induced by E2. Its site of action is suggested to be at the hypothalamic level, and its possible mechanism of action is discussed.

The synthesis and release of gonadotropins in response to gonadotropin-releasing hormone of the rat anterior pituitary gland during weight reduction

1990 ◽  
Vol 122 (5) ◽  
pp. 628-632 ◽  
Author(s):  
Fumikazu Kotsuji ◽  
Takeshi Aso ◽  
Naoyuki Kamitani ◽  
Toshiro Tominaga
Keyword(s):  
Weight Loss ◽  
Pituitary Gland ◽  
Weight Reduction ◽  
Female Rats ◽  
Serum Lh ◽  
Female Wistar Rats ◽  
Progressive Weight Loss ◽  
Lh Release ◽  
Lh Secretion

Abstract. It is well recognized that weight reduction produces the suppression of serum LH but not FSH level in rodents. In order to clarify the mechanism by which the discrepancy between LH and FSH levels is brought about, the influence of weight loss on the pituitary function was explored using female rats. The changes of the pituitary response to GnRH and the basal secretion of gonadotropins with progressive weight loss were investigated by in vitro short-term incubation of the pituitary gland after prolonged weight loss in female Wistar rats. On the first day of diestrous and until day 14 of the diet, GnRH induced LH and FSH release from the pituitary and a decrease in pituitary content of them, but the total amount of gonadotropin in culture medium and pituitary tissue was not affected. On day 30 of the diet, the decrease in pituitary content disappeared. On day 60 LH release disappeared, whereas pituitary FSH and the total amount of gonadotropins were increased by GnRH. Non-stimulated FSH but not LH secretion per mg of pituitary was augmented during dieting. The data indicate that pituitary responsiveness to GnRH and non-stimulated FSH release were modified by weight loss: the LH-releasing action of GmRH was diminished, the gonadotropin-synthesizing action of GnRH was augmented, and non-stimulated FSH release was increased.

Epidermal growth factor stimulates secretion of rat pituitary luteinizing hormone in vitro

1985 ◽  
Vol 108 (2) ◽  
pp. 175-178 ◽  
Author(s):  
Akira Miyake ◽  
Keiichi Tasaka ◽  
Shirou Otsuka ◽  
Hiroko Kohmura ◽  
Hiroshi Wakimoto ◽  
...  
Keyword(s):  
Growth Factor ◽  
Luteinizing Hormone ◽  
Epidermal Growth Factor ◽  
Female Rats ◽  
Gonadotrophin Secretion ◽  
Significant Release ◽  
Lh Release ◽  
Epidermal Growth ◽  
Lh Releasing Hormone

Abstract. The effects of epidermal growth factor (EGF) on pituitary luteinizing hormone (LH) release and on the releases induced by oestradiol (E2) and LH-releasing hormone (LRH) were examined in a sequential double chamber perifusion system. In this system the mediobasal hypothalami (MBH) and/or pituitaries excised from normally cycling female rats in dioestrus were perifused with test media. Perifusion with EGF at 1 ng/ml for 30 min induced significant release (80–100% increase, P <0.05) of LH from hypothalamo-pituitary pairs, but not from the pituitary alone. Perifusion of the pituitary alone with medium containing 1 ng/ml EGF, resulted in significant release of LH (70–140% increase, P < 0.05) after adminnistration of 10−7 m E2, but did not significantly influence LH release in response to 20 ng/ml LRH. These findings suggest that EGF may be involved in the regulation of pituitary gonadotrophin secretion by a direct effect on the hypothalamus and indirectly by increasing the pituitary responsiveness to E2.

scholarly journals  Steroid effects on the in vitro LH secretion from pituitary cells of sexually immature carp (Cyprinus carpio L.) under the influence of naltrexone and morphine

2010 ◽  
Vol 55 (No. 6) ◽  
pp. 250-257
Author(s):  
M. Sokolowska-Mikolajczyk ◽  
M. Socha ◽  
P. Epler
Keyword(s):  
Cyprinus Carpio ◽  
Sex Steroids ◽  
Pituitary Cells ◽  
Control Medium ◽  
Opioid Agonist ◽  
Carp Cyprinus Carpio ◽  
Lh Release ◽  
Lh Secretion

Dispersed cells from sexually immature carp (footlings) pituitaries were exposed to estradiol (E<sub>2</sub>) or testosterone (T) (both at 3 &times; 10<sup>&ndash;8</sup> M) in the presence of opioid receptor antagonist naltrexone (10<sup>&ndash;8</sup> or 10<sup>&ndash;6</sup> M) and/or agonist &ndash; morphine (10<sup>&ndash;8</sup> or 10<sup>&ndash;6</sup> M). Naltrexone alone at 10<sup>&ndash;6</sup> M increased the LH level as compared with the control. Morphine (10<sup>&ndash;8</sup> or 10<sup>&ndash;6</sup> M), T and E2 had no influence on LH levels. The combination of T with naltrexone (10<sup>&ndash;8</sup> M) stimulated LH release if compared with the control or with T alone. Morphine (both concentrations) with T caused significantly higher LH secretion than the control medium and T alone. Estradiol with naltrexone (10<sup>&ndash;8</sup> and 10<sup>&ndash;6</sup> M) had no influence on LH concentration. In media with E2 and morphine (10<sup>&ndash;8</sup> M) LH levels were higher than in the control and estradiol alone. The results show that in common carp sex steroids affect the response of pituitary cells to opioid agonist or antagonist giving an evidence on the role of steroids in LH release mediated by the opioid system.

Substance P stimulates gonadotropin-releasing hormone release from rat hypothalamus in vitro with involvement of oestrogen

1987 ◽  
Vol 115 (2) ◽  
pp. 247-252 ◽  
Author(s):  
Shirou Ohtsuka ◽  
Akira Miyake ◽  
Takamichi Nishizaki ◽  
Keiichi Tasaka ◽  
Toshihiro Aono ◽  
...  
Keyword(s):  
Substance P ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Normal Female ◽  
Dependent Manner ◽  
Gnrh Release ◽  
In Series ◽  
Significant Release ◽  
Lh Release

Abstract. The effects of substance P on the release of LH and GnRH were examined in a sequential double-chamber perifusion system by perifusing the medio-basal hypothalamus and/or pituitary excised from normal female rats in dioestrus or ovariectomized rats. When the medio-basal hypothalamus and pituitary from normal rats were perifused in series with substance P (10−6 mol/l), the concentration of LH in the efflux was significantly (P < 0.05) increased by 70– 120% compared with that before the injection, but substance P had no effect on LH release from the pituitary perifused alone. This LH release by substance P increased in a dose-dependent manner and was blocked by substance P antagonist. Administration of 10−6 mol/l substance P induced a significant release (40–80% increase, P < 0.05) of GnRH from the medio-basal hypothalamus. Infusion of 10−6 mol/l substance P induced significant release (50–100% increase, P < 0.05) of LH and GnRH in ovariectomized rats with an implanted oestradiol capsule, but caused no significant increase in LH release in ovariectomized rats without an oestradiol capsule. Progesterone injection to both ovariectomized rats and ovariectomized rats with an implanted oestradiol capsule had no significant effect on the response of LH to substance P. These findings suggest that substance P induces GnRH release from the medio-basal hypothalamus, resulting in LH release from the pituitary, and that oestrogen may be involved in these processes.

scholarly journals Effects of non-steroidal gonadal factors on LH secretion in female common carp during the reproductive cycle

2008 ◽  
Vol 53 (No. 9) ◽  
pp. 398-403
Author(s):  
J. Chyb ◽  
T. Mikolajczyk ◽  
M. Sokolowska-Mikolajczyk ◽  
M. Socha ◽  
P. Szczerbik ◽  
...  
Keyword(s):  
Common Carp ◽  
Reproductive Cycle ◽  
Inhibitory Effect ◽  
Gonad Maturity ◽  
Lh Release ◽  
Gonadal Recrudescence ◽  
Lh Secretion

The aim of this study was to evaluate the effects of recombinant human inhibin A, recombinant human activin A and desteroidized ovarian extract on LH secretion <I>in vitro</I> and <I>in vivo</I> in female common carp during different stages of reproductive cycle. Inhibin stimulated spontaneous as well as GnRH-stimulated LH release <I>in vivo</I> in fish during gonadal recrudescence. This hormone did not have an influence on spontaneous LH secretion in the periovulatory period, but had a slightly inhibitory effect on GnRH-stimulated LH release in this stage of gonad maturity. Activin decreased spontaneous LH secretion during gonadal recrudescence and increased LH secretion before ovulation, having no effects on GnRH-stimulated LH release during both stages of gonad maturity. The desteroidized ovarian extract failed to modify spontaneous LH secretion, but decreased GnRH-stimulated LH release during recrudescence and especially before ovulation. It is to conclude that these data suggest the differential role of inhibin/activin as substances in the regulation of LH secretion in common carp females.

Vasoactive intestinal peptide indirectly elicits pituitary LH secretion independent of GnRH in female zebrafish

Endocrinology ◽  
2022 ◽  
Author(s):  
Sakura Tanaka ◽  
Nilli Zmora ◽  
Berta Levavi-Sivan ◽  
Yonathan Zohar
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Mature Female ◽  
Mrna Levels ◽  
Lh Release ◽  
Lh Cells ◽  
Female Zebrafish ◽  
Lh Secretion ◽  
Sexually Mature

Abstract Vasoactive intestinal peptide (Vip) regulates luteinizing hormone (LH) release through the direct regulation of gonadotropin-releasing hormone (GnRH) neurons at the level of the brain in female rodents. However, little is known regarding the roles of Vip in teleost reproduction. Although GnRH is critical for fertility through the regulation of LH secretion in vertebrates, the exact role of the hypophysiotropic GnRH (GnRH3) in zebrafish is unclear since GnRH3 null fish are reproductively fertile. This phenomenon raises the possibility of a redundant regulatory pathway(s) for LH secretion in zebrafish. Here, we demonstrate that VipA (homologues of mammalian Vip) both inhibits and induces LH secretion in zebrafish. Despite the observation that VipA axons may reach the pituitary proximal pars distalis including LH cells, pituitary incubation with VipA in vitro, and intraperitoneal injection of VipA, did not induce LH secretion and lhβ mRNA expression in sexually mature females, respectively. On the other hand, intracerebroventricular administration of VipA augmented plasma LH levels in both wild type and gnrh3-/- females at 1 hour post-treatment, with no observed changes in pituitary GnRH2 and GnRH3 contents and gnrh3 mRNA levels in the brains. While VipA’s manner of inhibition of LH secretion has yet to be explored, the stimulation seems to occur via a different pathway than GnRH3, dopamine, and E2 in regulating LH secretion. The results indicate that VipA induces LH release possibly by acting with or through a non-GnRH factor(s), providing proof for the existence of functional redundancy of LH release in sexually mature female zebrafish.

Sign in / Sign up

Export Citation Format

Share Document