Role of serotoninergic neurones in the control of gonadotrophin and prolactin secretion in the rat

1982 ◽  
Vol 94 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Csilla Ruzsas ◽  
Patrizia Limonta ◽  
L. Martini
Keyword(s):  
Combined Treatment ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Intact Male ◽  
Prolactin Release ◽  
Lh Secretion ◽  
The Brain

The role of brain serotonin (5-hydroxytryptamine, 5-HT) in the control of LH, FSH and prolactin secretion was studied in two groups of experimental animals: intact adult male rats and ovariectomized adult female rats. 5-Hydroxytryptophan (5-HTP), a precursor of serotonin synthesis, and fluoxetine, a specific inhibitor of 5-HT uptake, were given either alone or together. 5-Hydroxytryptophan (50 mg/kg) was administered intraperitoneally and fluoxetine (20 μg/rat) was given into one of the lateral ventricles of the brain. Neither 5-HTP nor fluoxetine given alone affected LH secretion but combined treatment with the two drugs elicited a significant increase in serum LH levels in both intact male and ovariectomized female rats. Fluoxetine and 5-HTP, alone or together, did not modify FSH secretion in either kind of animal. In intact males and in ovariectomized females, 5-HTP induced a significant increase in prolactin release; fluoxetine alone was ineffective. In male animals treated with fluoxetine plus 5-HTP, serum prolactin levels increased but such an increase was lower than that found in the animals treated only with 5-HTP. In ovariectomized rats, the combined treatment induced an increase in serum prolactin levels similar to that found in animals treated with 5-HTP alone. These data suggested that brain serotonin exerts a stimulating effect on LH secretion in both intact male and ovariectomized rats, but that it does not play any role in the control of FSH release in either kind of animal and that central serotoninergic pathways participate in the stimulating control of prolactin release from the anterior pituitary gland. However, some of the data also suggested the possibility of the existence in the brain of serotoninergic systems inhibiting prolactin secretion.

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.

EVIDENCE OF ANTAGONISM BETWEEN PROLACTIN AND GONADOTROPHIN SECRETION: EFFECT OF METHALLIBURE ON PERPHENAZINE-INDUCED PROLACTIN SECRETION IN OVARIECTOMIZED RATS

1971 ◽  
Vol 51 (4) ◽  
pp. 719-725 ◽  
Author(s):  
M. BEN-DAVID ◽  
A. DANON ◽  
F. G. SULMAN
Keyword(s):  
Combined Treatment ◽  
Virgin Female ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Pituitary Cells ◽  
Similar Treatment ◽  
Gonadotrophin Secretion ◽  
High Doses

SUMMARY Perphenazine has previously been shown to stimulate prolactin secretion in intact and to a lesser degree in ovariectomized virgin female rats. The question whether the oversecretion of gonadotrophins (follicle-stimulating hormone and luteinizing hormone) occurring in ovariectomized animals interferes with the ability of the pituitary cells to secrete prolactin was investigated in sham-operated and ovariectomized rats after separate and combined treatment with methallibure (ICI-33828, a non-steroidal gonadotrophin suppressor) and perphenazine which served as a prolactin releaser. Pituitary and serum prolactin were measured simultaneously by radioimmunoassay. Serum prolactin detected at the end of 5 days' treatment with perphenazine (5 mg/kg/day, s.c.) was found to be increased (81 ng/ml) compared with controls (29 ng/ml). Similar treatment given to ovariectomized animals increased serum prolactin levels from 13·7 ng/ml to only 27 ng/ml. Although high doses of methallibure alone (20 mg/kg/day, s.c.) given to ovariectomized rats for 17 days restored prolactin secretion to the levels occurring in intact non-treated animals, a dose of 10 mg was ineffective. However, when 10 mg methallibure were given to perphenazine-treated ovariectomized rats, serum prolactin rose again to 80·1 ng/ml. These results provide substantial evidence that, when the pituitary is secreting high amounts of gonadotrophin, its prolactin secretion is reduced and its ability to secrete prolactin after perphenazine challenge is limited. Once the gonadotrophic oversecretion is suppressed, more prolactin is secreted and the pituitary can again secrete high amounts of prolactin when challenged by perphenazine. The results show that in rats there exists an antagonism between gonadotrophin and prolactin secretion.

Feedback regulation by progesterone of stress-induced prolactin release in rats

1989 ◽  
Vol 120 (1) ◽  
pp. 37-43 ◽  
Author(s):  
R. P. Deis ◽  
E. Leguizamon ◽  
G. A. Jahn
Keyword(s):  
Prolactin Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Serum Prolactin ◽  
Progesterone Concentration ◽  
Prolactin Release ◽  
Serum Progesterone ◽  
Progesterone Secretion ◽  
Male And Female Rats

ABSTRACT We have previously found that modifications to serum progesterone concentration have profound inhibitory effects on prolactin release in response to ether stress. The objective of the present study was to determine the effect of ether stress on progesterone secretion and the role of this steroid in ether-induced prolactin release. Serum progesterone concentration, 5 min after ether stress had been applied over a 2-min period, was consistently increased in male rats, in cyclic rats on the mornings of pro-oestrus and oestrus, and in androgenized rats in permanent oestrus. Ovariectomized androgenized rats showed the same response. Adrenalectomy of male and female rats abolished the progesterone increase induced by stress. Thus, the progesterone secreted by stressed rats is mostly of adrenal origin. In groups of male and pro-oestrous rats, circulating concentrations of prolactin and progesterone were measured from 5 to 60 min after stress. In both sexes the serum prolactin concentration was significantly increased at only 5 and 10 min after stress when compared with control values. In pro-oestrous rats the serum progesterone concentration was significantly higher than in controls at 5, 10 and 20 min after stress, whilst in male rats the concentration remained significantly higher at 30 min. Thirty minutes after the first stress, male and pro-oestrous rats were etherized for 2 min, and bled 5 min after removal from the ether container. In female rats this second stress produced only a slight but significant increase in serum prolactin concentrations, whereas in male rats prolactin concentrations did not increase. The second stress was still capable of significantly increasing circulating progesterone concentrations to levels similar to those obtained after the first stress in animals from all groups. Thus, an increased circulating progesterone concentration did not lead to regulation of further progesterone secretion. To find whether this type of response was due to a blocking effect of the previously released progesterone, animals were injected with the anti-progesterone RU 38486 (17β-hydroxy-11β-(4-dimethylaminophenyl)-17α-propinyl-oestra-4,9-dien-3-one) or with a specific antibody raised against progesterone. In both groups of treated rats the second stress induced a significant increase in serum prolactin and progesterone concentrations to give values similar to those obtained after the first stress. When the second stress was applied to female rats 60 min after the first the prolactin response was comparable to that obtained after the first exposure to ether. In conclusion, we have demonstrated that serum prolactin and progesterone concentrations are significantly increased after ether stress, and that the latter hormone exerts an inhibitory regulatory feedback on prolactin secretion. These results provide an important new insight into the role of progesterone in the regulation of prolactin release. Journal of Endocrinology (1989) 120, 37–43

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.

scholarly journals Temporal expression of estrogen receptor α in the hypothalamus and medulla oblongata during fasting: a role of noradrenergic neurons

2006 ◽  
Vol 190 (3) ◽  
pp. 593-600 ◽  
Author(s):  
Beverly A S Reyes ◽  
Hiroko Tsukamura ◽  
Helen I’Anson ◽  
Maria Amelita C Estacio ◽  
Kanjun Hirunagi ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Brain Regions ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Noradrenergic Neurons ◽  
Anatomical Relationship ◽  
Relationship Of ◽  
Lh Secretion

Fasting-induced LH suppression is augmented by estrogen in female rats. We investigated the temporal changes in the number of estrogen receptor α (ERα)-immunoreactive (ir) cells in various brain regions in ovariectomized rats fasted for 6, 24, 30, and 48 h, commencing at 1300 h. We also determined the anatomical relationship of ERα immunoreactivity and dopamine-β-hydroxylase (DBH) neurons in the A2 region of the nucleus of the solitary tract (NTS) and the paraventricular nucleus (PVN). The number of ERα-ir cells significantly increased after 30 h from the onset of fasting in the PVN and NTS compared with the unfasted controls and was sustained until 48 h. In the A2 region of 48-h fasted rats, 46.75% DBH-ir cells expressed ERα, and this was significantly higher than in unfasted controls (8.16% DBH-ir cells expressed ERα). In the PVN, most ERα-ir neurons were juxtaposed with DBH-ir varicosities. These results suggest that ERα is expressed in specific brain regions at a defined time from the onset of fasting. In addition, the anatomical relationship of noradrenergic and ERα-ir neurons in the A2 region and PVN may suggest a role for estrogen in increasing the activity of noradrenergic neurons in the A2 region and enhancing sensitivity of the PVN to noradrenergic input arising from the lower brainstem and thereby augmenting the suppression of LH secretion during fasting.

ROLE OF OESTROGENS AND GONADOTROPHINS IN PERPHENAZINE-INDUCED MAMMOGENESIS

1970 ◽  
Vol 48 (3) ◽  
pp. 365-371 ◽  
Author(s):  
A. DANON ◽  
C. P. WELLER ◽  
F. G. SULMAN
Keyword(s):  
Median Eminence ◽  
Mammary Glands ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Gonadotrophin Secretion

SUMMARY Treatment of intact or recently (1 day) ovariectomized female rats with 5 mg perphenazine (Trilafon)/kg/day for 5 days resulted in marked lobulo—alveolar differentiation of the mammary glands. Perphenazine failed to stimulate mammogenesis in chronically (12 days) ovariectomized rats, unless they had been primed with oestradiol. However, mammogenic effects in chronically ovariectomized rats were obtained after implantation of minute amounts (2 μg) of oestradiol into the median eminence, or after treatment for 16 days with the non-steroid pituitary gonadotrophin-inhibitor methallibure (ICI 33828; 20 mg/kg/day). Since these latter procedures counteract the gonadotrophin surge after ovariectomy, it would appear that inhibition of gonadotrophin secretion is necessary before prolactin secretion can be stimulated by perphenazine. Castrated male rats responded to perphenazine with lobulo—alveolar differentiation similar to that in intact males. The implications of this difference with regard to the mechanism of pituitary response to gonadectomy are discussed.

scholarly journals The Role of the Medial and Central Amygdala in Stress-Induced Suppression of Pulsatile LH Secretion in Female Rats

Endocrinology ◽  
2011 ◽  
Vol 152 (2) ◽  
pp. 545-555 ◽  
Author(s):  
Yuanshao Lin ◽  
Xiaofeng Li ◽  
Micol Lupi ◽  
James S. Kinsey-Jones ◽  
Bei Shao ◽  
...  
Keyword(s):  
Pulse Generator ◽  
Reproductive Function ◽  
Ibotenic Acid ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Inhibitory Effects ◽  
Cardiac Catheters ◽  
Response To Stress ◽  
Lh Secretion

Abstract Stress exerts profound inhibitory effects on reproductive function by suppressing the pulsatile release of GnRH and therefore LH. Although the mechanisms by which stressors disrupt the hypothalamic GnRH pulse generator remain to be fully elucidated, numerous studies have implicated the amygdala, especially its medial (MeA) and central nuclei (CeA), as key modulators of the neuroendocrine response to stress. In the present study, we investigated the roles of the MeA and CeA in stress-induced suppression of LH pulses. Ovariectomized rats received bilateral ibotenic acid or sham lesions targeting the MeA or CeA; blood samples (25 μl) were taken via chronically implanted cardiac catheters every 5 min for 6 h for the measurement of LH pulses. After 2 h of baseline sampling, the rats were exposed to either: restraint (1 h), insulin-induced hypoglycemia (IIH) (0.3 U/kg, iv), or lipopolysaccharide (LPS) (25 μg/kg, iv) stress. The restraint but not IIH or LPS stress–induced suppression of LH pulses was markedly attenuated by the MeA lesions. In contrast, CeA lesioning attenuated LPS, but not restraint or IIH stress–induced suppression of LH pulses. Moreover, after restraint stress, the number of Fos-positive neurons and the percentage of glutamic acid decarboxylase67 neurons expressing Fos was significantly greater in the GnRH-rich medial preoptic area (mPOA) of rats with intact, rather than lesioned, MeA. These data indicate that the MeA and CeA play key roles in psychogenic and immunological stress-induced suppression of the GnRH pulse generator, respectively, and the MeA-mediated effect may involve γ-aminobutyric acid ergic signaling within the mPOA.

Effects of orphanin FQ on central dopaminergic neuronal activities and prolactin secretion

2001 ◽  
Vol 280 (3) ◽  
pp. R705-R712 ◽  
Author(s):  
Kun-Ruey Shieh ◽  
Jenn-Tser Pan
Keyword(s):  
Receptor Gene ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Serum Prolactin ◽  
Antisense Oligodeoxynucleotide ◽  
Dependent Manner ◽  
Orphanin Fq ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
The Brain

Effects of orphanin FQ (OFQ) on central dopaminergic (DA) neurons and serum prolactin (PRL) were examined in ovariectomized, estrogen-primed Sprague-Dawley rats. The activities of central DA neurons, including the tuberoinfundibular (TI), nigrostriatal, mesolimbic, and incertohypothalamic ones, were determined by measuring the levels of 3,4-dihydroxyphenylacetic acid (DOPAC), the major metabolite of dopamine, in their projection regions in the brain by HPLC plus electrochemical detection. Intracerebroventricular administration of OFQ lowered DOPAC levels in the median eminence (ME), striatum, nucleus accumbens, and hypothalamic paraventricular nucleus in a dose (0.01–10 μg)- and time (30–90 min)-dependent manner. In contrast, OFQ increased DOPAC in the suprachiasmatic nucleus and had no effect in the periventricular nucleus. Serum PRL levels exhibited a typical inverse relationship with the activity of TIDA neurons, as determined by DOPAC levels in the ME. In the afternoon, we observed an endogenous decrease of ME DOPAC level accompanied by a PRL surge in estrogen-primed female rats. Although OFQ caused further decrease of ME DOPAC in the afternoon, it failed to augment the PRL surge level. Although pretreatment of an antisense oligodeoxynucleotide against the opioid receptor-like receptor gene had no effect on basal ME DOPAC levels in the morning or afternoon, it attenuated the afternoon PRL surge. Furthermore, it blocked the effects of exogenous OFQ on ME DOPAC and serum PRL levels, whereas the sense or missense oligodeoxynucleotide had no effect. These results indicate that OFQ and its receptors may be involved in the regulation of central DA neuronal activity and PRL secretion.

Sexual differences in the effect of serotonin on LH secretion in rats

1985 ◽  
Vol 109 (3) ◽  
pp. 320-325 ◽  
Author(s):  
Jaime A. Moguilevsky ◽  
María R. Faigón ◽  
Modesto C. Rubio ◽  
Pablo Scacchi ◽  
Berta Szwarcfarb
Keyword(s):  
Sexual Differences ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Adult Rats ◽  
Serotoninergic Neurons ◽  
Male And Female Rats ◽  
Lh Release ◽  
Prepubertal Rats ◽  
Lh Secretion ◽  
The Brain

Abstract. The effect of 5-hydroxytryptophan (5-HTP), a serotonin (5-HT) precursor, on luteinizing hormone (LH) secretion was studied in prepubertal male and female rats of different ages. In females 5-HTP stimulated LH release on days 16, 18 and 20 but not in older rats (26, 30, 35 days of age). No effects of 5-HTP on LH levels were observed in males. The positive feed-back mechanism of oestrogen-progesterone (E-P), that normally matures in the female between 20 and 26 days, was inhibited by 5-HTP in all the ages studied during prepuberty (26, 30 and 35 days old). On the other hand, in adult ovariectomized rats, 5-HTP administration not only decreased the high LH levels induced by ovariectomy, but the LH release response to E-P as well. These results indicate that there are sexual differences in the effect of 5-HT on LH in prepubertal rats younger than 26 days old. Administration of p-chloroamphetamine (PCA) a serotonin neurotoxin selective for serotoninergic neurons that depletes 5-HT levels in the brain, induced a significant increase in the LH release response to LRH in females, but had no effect in males. These results, besides suggesting a probable pituitary participation in the 5-HT action on LH secretion in the female, appear to indicate the existence of sexual differences in the effect of 5-HT in adult rats.

A physiological dose of estradiol with progesterone affects striatum biogenic amines

1990 ◽  
Vol 68 (12) ◽  
pp. 1520-1526 ◽  
Author(s):  
Marc Morissette ◽  
Daniel Lévesque ◽  
Alain Bélanger ◽  
Thérèse Di Paolo
Keyword(s):  
Steroid Injection ◽  
Acute Effect ◽  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Rat Striatum ◽  
Plasma Prolactin ◽  
Intact Male ◽  
Hydroxyindoleacetic Acid ◽  
The Brain

The acute effect of estradiol and progesterone on dopamine and serotonin metabolism in rat striatum was studied. One subcutaneous injection of 17β-estradiol (300 ng) and progesterone (150 μg) into intact male rats increased plasma levels of these steroids, while testosterone, corticosterone, and estrone remained unchanged. Dehydroepiandrosterone, androstane-3β, 17β-diol and dihydrotestosterone remained undetectably low. Prolactin decreased and androstane-3α,17β-diol, and 17-OH progesterone increased, but less than estradiol and progesterone. Peak levels of striatal dopamine, dihydroxyphenylacetic acid, and homovanillic acid were observed 15–45 min after steroid injection with a return to control values after 45–60 min, while serotonin and 5-hydroxyindoleacetic acid levels were slightly decreased. An injection of estradiol (70 ng) with progesterone (70μg) to ovariectomized female rats left plasma prolactin levels unchanged, while striatum dopamine and serotonin as well as their metabolite concentrations peaked 15–60 min after steroid injection and returned to control values after 45–75 min. To allow for a better comparison of the action of these steroids, the effect of estradiol or progesterone alone and in combination on the brain of ovariectomized rats was compared in the same experiment. A similar increase in metabolites of dopamine levels was observed after these steroids alone or in combination, while dopamine levels were increased only after progesterone alone or in combination with estradiol. An injection of estradiol or progesterone to ovariectomized rats led to peak steroid concentrations at approximately the same time in the brain and plasma. In addition, plasma and brain steroid levels were significantly correlated. Thus, levels of estradiol and progesterone that occur during the estrous cycle can rapidly increase striatum dopaminergic activity in rats of both sexes, while serotonin activity is increased only in female rats.Key words: estradiol, progesterone, striatum, dopamine, serotonin.

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