Cholinergic inputs to the amygdala and the control of gonadotrophin release

1980 ◽  
Vol 93 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Flavio Piva ◽  
José Borrell ◽  
Patrizia Limonta ◽  
Gilberto Gavazzi ◽  
Luciano Martini
Keyword(s):  
Nicotinic Receptors ◽  
Serum Levels ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Muscarinic Agonist ◽  
Time Intervals ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
Lh Secretion ◽  
Cholinomimetic Drugs

Abstract. Adult female rats castrated 4 weeks before were implanted bilaterally into the basomedial area of the amygdala with drugs known to mimic or to counteract the actions of acetylcholine. The animals were sacrificed at different time intervals after the implantation of the different compounds, and serum levels of LH and FSH were measured by radioimmunoasay. The data obtained indicate that the intra-amygdalar implantation of the muscarinic blocker atropine induces a significant increase of the release of LH without altering FSH secretion. The implantation of two cholinomimetic drugs, pilocarpine, an almost pure muscarinic agonist, and carbachol, which possesses both muscarinic and nicotinic properties, exerted an inhibitory effect only on LH release. On the contrary, the intra-amygdalar placement of the nicotinic blocker mecamylamine was followed by an increase of FSH with no changes in LH. These observations may suggest that cholinergic signals reaching the amygdala may be of some relevance in the mechanisms controlling gonadotrophin secretion. Muscarinic receptors seem to play an inhibitory role in the regulation of LH secretion, while nicotinic receptors seem to modulate in an inhibitory way FSH release.

Influence of anti-oestrogens on gonadotrophin secretion in control and ACTH-infused immature rats

1984 ◽  
Vol 105 (3) ◽  
pp. 308-313 ◽  
Author(s):  
David R. Mann ◽  
Michael S. Blank ◽  
R. Sridaran ◽  
V. Daniel Castracane ◽  
Charles Eldridge ◽  
...  
Keyword(s):  
Serum Testosterone ◽  
Serum Levels ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Constant Infusion ◽  
Simultaneous Treatment ◽  
Serum Lh ◽  
Gonadotrophin Secretion ◽  
Immature Rats ◽  
Lh Secretion

Abstract. The objective of this study was to determine whether anti-oestrogens (nafoxidine, MER-25) would block the suppressive effects of ACTH on gonadotrophin secretion in immature rats. Female rats were castrated at 25–26 days of age, and an Alzet osmotic minipump containing ACTH (1–24) or saline was implanted in each animal. ACTH was administered at a rate of 1 IU/day by constant infusion. Beginning on the day of surgery, animals were injected daily for 5 days with 0.25, 5 or 25 μg/100 g body weight of nafoxidine or 5 mg MER-25 and sacrificed on the sixth day following castration. ACTH lowered serum LH concentrations and increased pituitary LH levels. Serum androstenedione concentrations were more than two times greater in ACTH-infused than in control rats, but serum oestrone levels were not affected. Serum testosterone and oestradiol concentrations in ACTH-infused rats remained below levels of detection. Administration of 0.25 μg of nafoxidine prevented the suppressive effects of ACTH on serum LH. Serum levels of LH in these animals were comparable to saline-treated controls (418 ± 94 vs 443 ± 73 ng/ml). The two higher doses of nafoxidine and MER-25 were ineffective in suppressing the actions of ACTH on serum LH. MER-25 reduced serum LH values in both controls and ACTH-infused rats. Serum FSH concentrations were not altered by ACTH or nafoxidine treatment. MER-25 elevated pituitary FSH concentrations in both control and ACTH-infused rats. These data suggest that the inhibitory effect of ACTH on LH secretion in immature rats is mediated by an oestrogenic steroid, since this action can be blocked by simultaneous treatment with a low dose of the anti-oestrogen, nafoxidine.

ADRENERGIC INPUTS TO THE AMYGDALA AND THE CONTROL OF GONADOTROPHIN RELEASE

1979 ◽  
Vol 90 (3) ◽  
pp. 385-393 ◽  
Author(s):  
José Borrell ◽  
Flavio Piva ◽  
Luciano Martini
Keyword(s):  
Brain Stem ◽  
Dopamine Receptor ◽  
Serum Levels ◽  
Female Rats ◽  
Receptor Blocker ◽  
Dopaminergic Drug ◽  
Gonadotrophin Secretion ◽  
Biphasic Effect ◽  
Adrenergic Blocker ◽  
The Brain

ABSTRACT Drugs able to mimic or to antagonize the action of catecholamines have been implanted bilaterally into the basomedial region of the amygdala of adult castrated female rats. The animals were killed at different intervals after the implantation of the different drugs, and serum levels of LH and FSH were measured by radioimmunoassay. The results have shown that the intra-amygdalar implantation of the alpha-adrenergic blocker phenoxybenzamine induces a significant increase of the release both of LH and FSH. The implantation of the beta-adrenergic blocker propranolol brings about a rise of LH only. The dopamine receptor blocker pimozide stimulates the release of LH and exerts a biphasic effect (stimulation followed by inhibition) of FSH secretion. The alpha-receptor stimulant clonidine and the dopaminergic drug 2-Br-alpha-ergocryptine were without significant effects. From these observations it is suggested that the adrenergic signals reaching the basomedial area of the amygdala (possibly from the brain stem) may be involved in the modulation of gonadotrophin secretion.

Effect of low doses of continuously administered catecholoestrogens on peripheral and central target organs

1981 ◽  
Vol 96 (4) ◽  
pp. 470-474 ◽  
Author(s):  
Peter Ball ◽  
Günter Emons ◽  
Ulrich Gethmann
Keyword(s):  
Serum Levels ◽  
Female Rats ◽  
Low Doses ◽  
Vaginal Opening ◽  
Uterine Weight ◽  
Central Target ◽  
Male And Female Rats ◽  
Target Organs ◽  
Uterine Growth ◽  
Lh Release

Abstract. Osmotic minipumps containing low doses of either 4-hydroxyoestradiol or 2-hydroxyoestradiol2) were sc implanted for 152 h (6⅓ day) into immature male and female rats. At the end of the test period the animals were killed and the uterine weight, the vaginal opening, the gonadotrophin serum levels and the gonadal weight monitored. The following results were obtained: 1) a significant increase in the uterine weight and a consistent vaginal opening were observed after 4-hydroxyoestradiol but not after 2-hydroxyoestradiol treatment, 2) LH-levels increased after 2-hydroxyoestradiol but not after 4-hydroxyoestradiol; the increase was, however, not significant, 3) FSH-levels and gonadal weights were lowered by 4-hydroxyoestradiol treatment in male animals only; 2-hydroxyoestradiol had no effect on FSH-levels in both sexes, 4) in no instance an antioestrogenic effect of either catecholoestrogen was observed. It is concluded that 4-hydroxyoestrogens — using the above paradigm — have a significant importance on uterine growth and vaginal opening but (on day 6) no role on LH-release, whereas 2-hydroxyoestrogens may increase LH levels (on day 6) but are nearly ineffective with respect to peripheral parameters.

scholarly journals Effect of androgen on Kiss1 expression and luteinizing hormone release in female rats

2017 ◽  
Vol 233 (3) ◽  
pp. 281-292 ◽  
Author(s):  
Kinuyo Iwata ◽  
Yuyu Kunimura ◽  
Keisuke Matsumoto ◽  
Hitoshi Ozawa
Keyword(s):  
Luteinizing Hormone ◽  
Arcuate Nucleus ◽  
Female Rats ◽  
Hormone Release ◽  
Lh Surge ◽  
Continuous Release ◽  
Ovulatory Dysfunction ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion

Hyperandrogenic women have various grades of ovulatory dysfunction, which lead to infertility. The purpose of this study was to determine whether chronic exposure to androgen affects the expression of kisspeptin (ovulation and follicle development regulator) or release of luteinizing hormone (LH) in female rats. Weaned females were subcutaneously implanted with 90-day continuous-release pellets of 5α-dihydrotestosterone (DHT) and studied after 10 weeks of age. Number of Kiss1-expressing cells in both the anteroventral periventricular nucleus (AVPV) and arcuate nucleus (ARC) was significantly decreased in ovary-intact DHT rats. Further, an estradiol-induced LH surge was not detected in DHT rats, even though significant differences were not observed between DHT and non-DHT rats with regard to number of AVPV Kiss1-expressing cells or gonadotrophin-releasing hormone (GnRH)-immunoreactive (ir) cells in the presence of high estradiol. Kiss1-expressing and neurokinin B-ir cells were significantly decreased in the ARC of ovariectomized (OVX) DHT rats compared with OVX non-DHT rats; pulsatile LH secretion was also suppressed in these animals. Central injection of kisspeptin-10 or intravenous injection of a GnRH agonist did not affect the LH release in DHT rats. Notably, ARC Kiss1-expressing cells expressed androgen receptors (ARs) in female rats, whereas only a few Kiss1-expressing cells expressed ARs in the AVPV. Collectively, our results suggest excessive androgen suppresses LH surge and pulsatile LH secretion by inhibiting kisspeptin expression in the ARC and disruption at the pituitary level, whereas AVPV kisspeptin neurons appear to be directly unaffected by androgen. Hence, hyperandrogenemia may adversely affect ARC kisspeptin neurons, resulting in anovulation and menstrual irregularities.

Plasma β-endorphin and LH during prolonged hypoglycaemia in ewes

1993 ◽  
Vol 1993 ◽  
pp. 93-93 ◽  
Author(s):  
A.M.X. Eloy ◽  
R.G. Rodway
Keyword(s):  
Plasma Concentrations ◽  
Reproductive Function ◽  
Opioid Peptide ◽  
Inhibitory Effect ◽  
Elevated Plasma ◽  
Lh Release ◽  
Lh Secretion

Normal reproductive function in female animals can be drastically impaired by a variety of stressful stimuli. For example, undernutrition and hypoglycaemia in sheep have been shown to suppress pulsatile LH secretion and to reduce the number of ewes showing pre-ovulatory LH peaks (Crump and Rodway 1986, Clarke et al. 1990). Similar stresses are also known to cause release of the opioid peptide β-endorphin into the circulation. Opioids are well-known to have a central inhibitory effect on LH release, although whether the elevated plasma concentrations of these peptides have any effect on LH secretion is unclear. The present study investigated the affect of insulin-induced hypoglycaemia on plasma concentrations of β-endorphin and LH.

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.

Effects of ovarian hormones on brain opioid binding sites in castrated female rats

1992 ◽  
Vol 263 (3) ◽  
pp. E507-E511 ◽  
Author(s):  
D. Dondi ◽  
P. Limonta ◽  
R. Maggi ◽  
F. Piva
Keyword(s):  
Negative Feedback ◽  
Positive Feedback ◽  
Binding Sites ◽  
Serum Levels ◽  
Estradiol Benzoate ◽  
Inhibitory Effect ◽  
Feedback Effect ◽  
Female Rats ◽  
Opioid Binding ◽  
Positive Feedback Effect

These experiments were performed to analyze whether treatments of ovariectomized female rats with ovarian steroid regimens able to induce either an increase (positive feedback effect) or a decrease (negative feedback effect) of serum levels of luteinizing hormone (LH) have some impact on the characteristics of mu-opioid binding sites in circumscribed areas of the brain. The increase of serum levels of LH elicited by a treatment with estradiol benzoate (EB) plus progesterone (P; positive feedback effect) was accompanied by a significant decrease in the number of mu-binding sites in the hypothalamus and in the corpus striatum. The decrease in serum levels of LH induced by a treatment with EB alone (negative feedback effect) brought about a significant increase of the number of mu-binding sites in the thalamus and in the hippocampus. These results seem to suggest that the release of LH induced by EB plus P may involve a decrease of hypothalamic mu-binding sites. Apparently, the inhibitory effect on LH release exerted by EB alone does not involve any change of the density of these binding sites in the hypothalamus.

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

Flurothyl-induced convulsions delay the onset of sexual maturation in the female rat

1982 ◽  
Vol 95 (1) ◽  
pp. 37-41 ◽  
Author(s):  
M. Wilkinson ◽  
R. Bhanot ◽  
J. A. Pincock ◽  
L. Donald
Keyword(s):  
Sexual Maturation ◽  
Serum Levels ◽  
Female Rats ◽  
Female Rat ◽  
Basal Serum ◽  
Age Related ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Related Increase

We have investigated whether sexual maturation in female rats is affected by repeated flurothyl-induced convulsions. This treatment had no effect on the normal age-related increase in body weight though puberty (vaginal opening) was significantly delayed when compared with non-convulsed control rats. In an attempt to probe the mechanism of this delaying effect we observed that (1) anterior pituitary response to gonadotrophin releasing hormone in vitro was normal in terms of LH release but FSH secretion was impaired and (2) progesterone injection in oestrogen-primed convulsed rats failed to generate an ovulatory-type surge of LH or FSH. Basal serum levels and basal in-vitro secretion of LH and FSH were normal. We conclude that repeated convulsions adversely affect the hypothalamo-pituitary-gonadotrophin system of immature female rats.

ACUTE EFFECTS OF HYPOTHALAMIC LESIONS UPON GONADOTROPHIN SECRETION IN THE FERRET

1981 ◽  
Vol 89 (3) ◽  
pp. 329-336 ◽  
Author(s):  
B. T. DONOVAN ◽  
M. B. TER HAAR
Keyword(s):  
Platinum Electrodes ◽  
Acute Effects ◽  
Hypothalamic Lesions ◽  
Gonadotrophin Secretion ◽  
Lh Release ◽  
High Concentrations ◽  
Lh Secretion ◽  
Steel Electrodes

The changes in FSH and LH secretion after placement of lesions in the hypothalamus were traced in ferrets serially bled at 15 min intervals. Passage of the lesioning current through platinum electrodes in anoestrous females was associated with an immediate surge in LH and FSH output. Damage to the hypothalamus of oestrous females also caused an immediate surge of LH secretion, but then a long-lasting second rise in blood LH content set in. High concentrations of LH were never sustained overnight. The response of long-term spayed females to the placement of hypothalamic lesions was similar to that of anoestrous ferrets, while that of anoestrous or oestrous ferrets was not altered by acute removal of the ovaries. Manipulation of the ovaries appeared to facilitate FSH and LH secretion. The response of males was similar to that of anoestrous females. Marked increases in FSH and LH release were also seen in females when lesions were made with steel electrodes, but had subsided on the following day.

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