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.

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.

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

EFFECTS OF NALOXONE ON LUTEINIZING HORMONE AND PROLACTIN IN SERUM OF RATS

1980 ◽  
Vol 85 (2) ◽  
pp. 307-315 ◽  
Author(s):  
M. S. BLANK ◽  
A. E. PANERAI ◽  
H. G. FRIESEN
Keyword(s):  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Immature Female ◽  
Subcutaneous Injections ◽  
Serum Lh ◽  
Opiate Peptides ◽  
Lh Release ◽  
Lh Secretion

The effects of subcutaneous injections of the opiate antagonist naloxone on the tonic and phasic secretion of prolactin and LH were studied in rats. During development, resting levels of prolactin in serum were decreased by naloxone (2·5 mg/kg body wt) on days 24,45 and 50 in female rats and on days 28,45 and 50 in male rats. In the adult, naloxone (2·5 mg/kg body wt) decreased basal levels of serum prolactin in male rats and levels during oestrus in female rats. In 25-day-old female rats, serum LH rose from resting levels within 7·5 min of naloxone administration (2·5 mg/kg body wt) and returned to pretreatment levels by 30 min, while prolactin fell by 7·5 min and remained low for as long as 60 min after treatment. Furthermore, a tenfold lower dose of naloxone (0·25 mg/kg body wt) did not raise basal levels of serum LH but still decreased resting levels of serum prolactin in immature female rats (24 days old). The effect of naloxone (2·5 mg/kg body wt) on phasic LH release was studied in 29-day-old immature female rats primed on day 27 with pregnant mare serum gonadotrophin (PMSG). In these PMSG-treated rats the onset of the prolactin surge was blunted by naloxone while it had no effect on phasic LH release. Naloxone (5 mg/kg body wt) also induced a rise in levels of serum LH in ovariectomized rats and, if administered with morphine, it reversed the short-term inhibition of LH secretion caused by morphine. However, naloxone was ineffective after pretreatment with oestradiol benzoate. These findings suggest that the responses of serum LH and prolactin to naloxone were dissociated and that oestrogens and opiate peptides may have interacted to regulate secretion of LH.

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.

Effects of treatment with the opioid antagonists naloxone and naltrexone on LH secretion and on sexual maturation in immature female rats

1988 ◽  
Vol 117 (2) ◽  
pp. 237-243 ◽  
Author(s):  
H. M. A. Meijs-Roelofs ◽  
P. Kramer
Keyword(s):  
Opioid Receptor ◽  
Sexual Maturation ◽  
Female Rats ◽  
Opioid Antagonists ◽  
Short Term ◽  
Neonatal Treatment ◽  
Serum Lh ◽  
Naltrexone Treatment ◽  
Lh Release ◽  
Lh Secretion

ABSTRACT The effects on sexual maturation of the opioid receptor antagonists naloxone and naltrexone were studied in the female rat. Neonatal treatment (days 1–10) with either naloxone (2·5 mg/kg at 6-h intervals) or naltrexone (20 or 50 mg/kg per day) did not advance sexual maturation as judged by age and body weight at vaginal opening and first ovulation. After treatment with naltrexone (20 mg/kg) first ovulation occurred 2·3 days earlier than in saline-treated control rats but this could be attributed to a growth-stimulating effect of naltrexone; the effect was not observed with 50 mg/kg. An effect of neonatal treatment with naloxone on serum LH levels was seen at 23 days of age (155±36 (s.e.m.) vs 14±4 μg LH/1 in controls, P<0·01), but not at 29 or 33 days of age, at 2 days before first ovulation nor at first pro-oestrus. There were no differences in the number of ova released at first oestrus, nor in the length of the first cycle. Neonatal treatment with naltrexone (50 mg/kg per day) did not alter the response to treatment with human chorionic gonadotrophin at 28–31 days of age: ovulation of a mean of 7·3 ova was induced on day 32 in both naltrexone- and saline-treated rats. Naltrexone treatment (four daily injections of 20 mg/kg at 2-h intervals) at 28–32 days of age advanced first ovulation by 4·4 days in about 40% of the rats. Short-term effects of naloxone and naltrexone treatment on LH secretion were studied in 15-day-old rats and a clear increase in serum LH concentration was seen 15 min after injection; LH levels were similar with the various doses of antagonist used (2·5 and 20 mg naloxone/kg; 2·5, 20 and 50 mg naltrexone/kg). At 30 min after injection LH levels were still maximal if the 2·5 mg/kg dose of either antagonist was used, whereas with the higher doses a significant (P<0·01) decrease in the level of LH was observed, indicating a longer-lasting effect of the lower (2·5 mg/kg) dose of antagonist on LH secretion. No differences in effectiveness were seen between the supposedly short-lasting opioid receptor antagonist naloxone and the supposedly long-lasting antagonist naltrexone. It was concluded that neonatal treatment with the opioid antagonists naloxone and naltrexone did not specifically influence sexual maturation. The antagonists clearly increased LH secretion in short-term experiments. Treatment with naltrexone at 28–32 days of age advanced first ovulation in 40% of the rats, a result that is in agreement with a possible opiatergic influence on the gradually increasing LH release during the final phase of sexual maturation. The effects of the opioid antagonist naltrexone on the LH release mechanism did not parallel its reported long-lasting effects on nociceptive response, no long-lasting increase of LH release was seen, and the timecourse of the LH response was the same using the antagonists naloxone and naltrexone. J. Endocr. (1988) 117, 237–243

The effect of D-Trp6-LRH upon secretion of gonadotrophin – a possible therapeutic application in anorexia nervosa

1984 ◽  
Vol 105 (2) ◽  
pp. 161-166 ◽  
Author(s):  
S. Zgliczyński ◽  
B. Baranowska ◽  
W. Jeske ◽  
A. Niewiadomska ◽  
G. Rozbicka ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Anorexia Nervosa ◽  
Prolactin Secretion ◽  
Control Group ◽  
Female Patients ◽  
Serum Lh ◽  
Normal Body Weight ◽  
Lh Release ◽  
Lh Secretion

Abstract. The aim of this study was to evaluate the effect of the agonistic LRH analogue (D-Trp6-LRH) on LH, FSH and prolactin secretion, and its possible efficacy in female patients with anorexia nervosa. The study included 18 female patients with anorexia nervosa and 7 healthy women in the same age group. The patients with anorexia nervosa were divided into two groups of 9 women each. The first group consisted of patients in the weight loss phase of the disorder and the second of 9 women who had achieved normal body weight. Additionally, in 6 women with anorexia nervosa serum LH concentration was determined in response to native LRH before and 14 days after the treatment with D-Trp6-LRH. Serum LH, FSH, prolactin concentrations were determined before and 5, 10, 24 and 48 h after administration of D-Trp6-LRH in a dose of 5 μg. The serum LH response to D-Trp6-LRH in the second group did not differ from that of the control group. However, in women with anorexia nervosa in the weight loss phase, LH release in response to administration of the analogue was significantly lower. FSH release after LRH analogue administration in both groups of patients with anorexia nervosa did not differ from that in the control group. The increased LH secretion in response to native LRH after treatment indicates that D-Trp6-LRH in low doses did not inhibit pituitary responsiveness. A dose of 5 μg of D-Trp6-LRH was administered in a therapeutic regimen every 48 h from 1 to 3 months to 7 of 9 patients with anorexia nervosa who exhibited amenorrhoea in spite of normalization of body weight. All the patients treated with the analogue resumed menstruation. The results of this study suggest that D-Trp6-LRH may be of value in the treatment of amenorrhoea in women with anorexia nervosa.

Suppression by LRH of the stimulatory effect of oestradiol on the secretion of LH by the rat pituitary gland

1987 ◽  
Vol 114 (4) ◽  
pp. 488-496
Author(s):  
G. A. Schuiling ◽  
H. Moes ◽  
J. de Koning ◽  
T. R. Koiter
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Secretion Rate ◽  
Ovariectomized Rats ◽  
Release Mechanisms ◽  
Lh Release ◽  
Lh Secretion ◽  
Positive Effect

Abstract. Ovariectomized rats were infused with varying doses of luteinizing hormone-releasing-hormone (LRH). Some of the rats were also treated with oestradiol benzoate (EB). The effects of these pre-treatments on the in vitro release of luteinizing hormone (LH) were studied. The following parameters of in vitro LH release were measured: a) the autonomous secretion rate; b) the secretion rate following maximum stimulation with LRH, and c) the total quantity of LH released during the 6-hour experiment. The in vivo pre-treatments with LRH and EB dose-dependently decreased the pituitary LH content as well as all three of the above parameters of in vitro LH secretion. There was a linear relationship between the pituitary LH content and the three parameters of in vitro LH release. These parameters were therefore expressed as percentage of the pituitary LH content to give the relative LH secretion rates. The three parameters were thereby corrected for LRH/EB-induced changes in the pituitary LH content. In this way we obtained information on the effects of LRH and EB on the state of the LH release mechanisms of the gonadotropes. EB potentiated the LRH-induced depletion of the pituitary LH stores at all in vivo LRH infusion rates. The effect of EB on the quantity of LH released during perifusion in vitro, however, varied with the previous LRH infusion rates. After LRH infusion rates lower than about 120 ng/h (which establishes plasma concentrations of about 70 ng/l) EB enhanced the stimulated quantity of LH released. After higher rates of LRH infusion, EB lowered the amount of LH released. The effect of EB on the relative secretion of LH in vitro, i.e. on the LH release mechanisms, however, was positive irrespective of the prior in vivo LRH infusion rates, although the effect of EB was greater at the lower rates of LRH infusion. The effect of EB on the autonomous, in vitro, LH secretion rate was positive irrespective of the prior in vivo LRH infusion rates. The positive effect of EB on the mechanism underlying this component of LH secretion was LRH-independent. The effect of EB on the mechanism underlying the LRH-stimulated component of LH release appeared to be strongly LRH-dependent. The effect of EB was maximal if the LRH infusion rate had been lower than about 50 ng/h. With higher infusion rates it became increasingly smaller and was zero at the rate of about 180 ng/h or more. The LRH infusion rates of 50 and 180 ng/h establish plasma LRH concentrations of about 30 and 90 ng/l. Thus, the positive effect of EB on the LRH-stimulated component of LH secretion can be regulated by LRH at the plasma concentration interval of 30–90 ng/l. This study demonstrates that the 'overall' effect of EB on the LH secretion rate is determined by the 'balance' between the effect of EB on the pituitary LH content (the potentiation of the LRH-induced depletion of the LH stores) and the effect of EB on the LH release mechanisms (which effect, in the case of the LRH-stimulated component of LH secretion, can be suppressed by LRH). If the former effect dominates, the effect of EB on the secretion of LH is negative, if the latter dominates, the effect of EB is positive. The LRH concentration at which the positive effect turns into the negative effect is about 70 ng/l. We suggest that the ability of LRH and EB to influence each others' effect on the pituitary gland at physiological concentrations of the two hormones, plays a role in the regulation of the secretion of LH.

Are catechol oestrogens obligatory mediators of oestrogen action in the central nervous system? II. Potencies of natural and synthetic oestrogens for induction of gonadotrophin release and female sexual behaviour in the rat

1986 ◽  
Vol 110 (3) ◽  
pp. 499-505 ◽  
Author(s):  
N. J. MacLusky ◽  
L. C. Krey ◽  
B. Parsons ◽  
G. R. Merriam ◽  
D. L. Loriaux ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Sexual Behaviour ◽  
Female Rats ◽  
Oestrogen Receptors ◽  
Ability To Act ◽  
The Central Nervous System ◽  
Lh Release ◽  
Lh Secretion ◽  
The Brain

ABSTRACT The role of catechol oestrogen formation in the mechanism by which circulating oestrogens facilitate gonadotrophin release and female sexual behaviour was explored in adult female rats. The effects of oestradiol-17β were compared with those of a group of oestrogens with either a reduced affinity for oestrogen receptors (oestradiol-17α) or a reduced ability to act as substrates for catechol oestrogen formation (2-fluoro-oestradiol, 4-fluoro-oestradiol and moxestrol (11β-methoxy-17α-ethynyloestradiol)). Rats were ovariectomized on the evening of dioestrus day 1 of the 4-day oestrous cycle and implanted s.c. 12 h later with infusion pumps containing either one of the test oestrogens or vehicle alone. Infusion rates for oestradiol-17β, moxestrol, 2-fluoro-oestradiol and 4-fluoro-oestradiol were adjusted to give concentrations of nuclear oestrogen receptors in the brain and pituitary gland within the range of those found in intact female rats during pro-oestrus. Oestradiol-17α was infused at the same and at a tenfold higher rate than that of oestradiol-17β; neither of these treatments with oestradiol-17α significantly increased brain or pituitary gland nuclear oestrogen receptor levels. On the day after the pump was implanted, samples of tail vein blood were withdrawn at 12.00, 14.00, 16.00 and 18.00 h for LH assay. All animals were then injected s.c. with 1 mg progesterone in propylene glycol, and tested for feminine sexual behaviour 5 h later. Oestradiol-17β, moxestrol, 2-fluoro-oestradiol and 4-fluoro-oestradiol all elicited pronounced LH surges and facilitated progesterone-triggered proceptive and lordosis behaviours. In contrast, oestradiol-17α was without effect on LH secretion and sexual behaviours. These results are consistent with the hypothesis that catechol oestrogen biosynthesis is not an obligatory step in the mechanism by which circulating oestrogens induce LH release and feminine sexual behaviour in the rat. J. Endocr. (1986) 110, 499–505

Changes in the characteristics of pulsatile luteinizing hormone secretion during the oestrous cycle and after ovariectomy and oestrogen treatment in female rats

1982 ◽  
Vol 94 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Takashi Higuchi ◽  
Masazumi Kawakami
Keyword(s):  
Hormone Secretion ◽  
Pulse Amplitude ◽  
Pulse Frequency ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Luteinizing Hormone Secretion ◽  
Oestrogen Treatment ◽  
Serum Lh ◽  
Lh Release

Changes in the characteristics of LH secretory pulses in female rats were determined in different hormonal conditions; during the oestrous cycle and after ovariectomy and oestrogen treatment. The frequency and amplitude of the LH pulses were stable during the oestrous cycle except at oestrus when a pattern could not be discerned because of low LH concentrations. These were significantly lower than those measured during other stages of the cycle. Mean LH concentrations and LH pulse amplitudes increased with time up to 30 days after ovariectomy. The frequency of the LH pulse was unchanged 4 days after ovariectomy when mean LH levels had already increased. The frequency increased 10 days after ovariectomy and then remained stable in spite of a further increase in mean serum LH concentrations. Oestradiol-17β injected into ovariectomized rats caused a decrease in LH pulse amplitude but no change in pulse frequency. One day after treatment with oestradiol benzoate no LH pulse was detectable, probably because the amplitude was too small. A generator of pulsatile LH release is postulated and an oestrogen effect on its function is discussed.

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.

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