Role of the uterine cervix in inhibition of sexual behaviour in lactating rats

1985 ◽  
Vol 106 (2) ◽  
pp. 183-188 ◽  
Author(s):  
G. Forsberg ◽  
P. Södersten ◽  
P. Eneroth
Keyword(s):  
Sexual Behaviour ◽  
Uterine Cervix ◽  
Subsequent Treatment ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Serum Progesterone ◽  
Concurrent Treatment ◽  
Lordosis Behaviour ◽  
Cervical Stimulation

ABSTRACT Treatment of ovariectomized rats with progesterone-filled constant-release implants, which increased serum progesterone concentrations to 99·4 ±5·0 nmol/l, facilitated the induction of lordosis behaviour by subsequent treatment with oestradiol benzoate (OB, 10 μg). Concurrent treatment with the dopamine receptor antagonist domperidone (two daily injections of 2·5 mg/rat), which increased serum prolactin concentrations, did not inhibit the behavioural response of ovariectomized progesterone-treated rats to OB. If the treatment was combined with stimulation of the uterine cervix it inhibited lordosis to a level which was comparable with that of progesterone–domperidone-treated rats, which had been ovariectomized and from which the pups had been removed on the day of parturition. The cervical stimulation did not increase the amount of prolactin secreted by the pituitary gland in response to an injection of domperidone. The behavioural effect of cervical stimulation was blocked by injecting an anaesthetic paste (0·1 ml lidocain–prilocain) intravaginally against the cervix. The effect of cervical stimulation, or of parturition, lasted only for a few days and sexual behaviour was inhibited during a prolonged period of lactation. Sucking by the pups on the nipples of the mother may be required for preventing sexual behaviour during the entire period of lactation. J. Endocr. (1985) 106, 183–188

Naloxone stimulates sexual behaviour in lactating rats

1987 ◽  
Vol 113 (3) ◽  
pp. 423-427 ◽  
Author(s):  
G. Forsberg ◽  
P. Eneroth ◽  
P. Södersten
Keyword(s):  
Receptor Antagonist ◽  
Sexual Behaviour ◽  
Opioid Peptide ◽  
Response To Treatment ◽  
Ovariectomized Rats ◽  
Serum Progesterone ◽  
Dopamine Receptor Antagonist ◽  
Peptide Receptor ◽  
Oestradiol Benzoate ◽  
Cervical Stimulation

ABSTRACT During lactation the display of sexual receptivity in response to treatment with oestradiol benzoate (OB; 2 or 10 μg) and progesterone (0·5 mg) was inhibited, but the behaviour could be activated by i.p. (5 mg) or intracerebroventricular (i.c.v.; 100 μg) but not intrathecal (i.t.; 100 or 500 μg) injections of the opioid peptide receptor antagonist naloxone. The behaviour was also inhibited in ovariectomized rats in which serum progesterone and prolactin levels had been raised by treatment with progesterone implants and the dopamine receptor antagonist domperidone, and the uterine cervix had been stimulated. Intraperitoneal injections of naloxone (1 mg) reactivated the behaviour of cervically stimulated rats. The concentration of β-endorphin-like immunoreactivity in the serum of lactating rats (42·8± 9·2 pmol/l) was not raised above that of ovariectomized rats (35·8 ± 8·4 pmol/l) nor was the concentration of β-endorphin-like immunoreactivity altered in the pituitary gland (22·5 ± 2·5 pmol/l), midbrain central grey (6·3 ± 2·2 pmol/l) or hypothalamus (5·6± 2·6 pmol/l) of lactating rats in comparison with ovariectomized rats (24·8 ± 4·4, 4·0 ± 2·0 and 4·7 ± 1·4 pmol/l respectively). Adrenalectomy facilitated the display of sexual behaviour in lactating rats treated with OB plus progesterone and caused a slight increase in serum β-endorphin-like immunoreactivity (30·5± 2·7 pmol/l) compared with that in non-adrenalectomized lactating rats (26·1 ± 2·1 pmol/l). It is suggested that an opioid peptide, but probably not β-endorphin, inhibits sexual behaviour during lactation and after cervical stimulation. J. Endocr. (1987) 113, 423–427

Activation of sexual behaviour in castrated rats: the role of oestradiol

1986 ◽  
Vol 111 (3) ◽  
pp. 455-462 ◽  
Author(s):  
P. Södersten ◽  
P. Eneroth ◽  
T. Hansson ◽  
A. Mode ◽  
D. Johansson ◽  
...  
Keyword(s):  
Sexual Behaviour ◽  
Reductase Inhibitor ◽  
Low Dose ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
High Dose ◽  
Hypothalamic Tissue ◽  
Lordosis Behaviour

ABSTRACT Sexual behaviour was induced in castrated male rats with oestradiol-17β- or testosterone-filled constant-release implants. Testosterone-induced sexual behaviour was unaffected by treatment with the 5α-reductase inhibitor 17β-N,N-diethylcarbamoyl-4-aza-5α-androstan-3-one (4-MA; 16·7 mg/day) but treatment with the aromatization inhibitor 1,4,6-androstatriene-3,17-dione (ATD; 10 mg/day) prevented testosterone from inducing the behaviour. Sexual behaviour could be activated in castrated rats treated with testosterone plus ATD by treatment with 4-MA or with implants filled with a low dose of oestradiol. Lordosis behaviour induced in ovariectomized rats with testosterone-filled implants and progesterone was blocked by ATD treatment and could not be activated with 4-MA but oestradiol implants restored the display of lordosis in the testosterone plus ATD-treated females. 4-MA inhibited the in-vitro formation of [14C]5α-dihydrotestosterone from [14C]testosterone by combined preoptic and hypothalamic tissue at all doses tested and a high dose of oestradiol exerted a similar effect. The results suggest that androgen aromatization is required for testosterone-activated female sexual behaviour but not for testosterone-activated male sexual behaviour. It is suggested that oestradiol normally acts to control the sexual behaviour of male rats by modifying neural androgen metabolism. J. Endocr. (1986) 111, 455–462

Adrenal progesterone facilitates the negative feedback of oestrogen on LH release in ovariectomized rats

1993 ◽  
Vol 139 (2) ◽  
pp. 253-258 ◽  
Author(s):  
A. M. Salicioni ◽  
R. W. Carón ◽  
R. P. Deis
Keyword(s):  
Ovariectomized Rats ◽  
Adrenal Steroids ◽  
Serum Progesterone ◽  
Oestrogen Treatment ◽  
Ovx Rats ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion

ABSTRACT There is evidence that the adrenals play a role in the regulation of the synthesis and release of gonadotrophins in various vertebrates. The aim of this study was to determine the part played by adrenal steroids, with special reference to progesterone, on the concentration of LH in ovariectomized (OVX) and oestrogen-primed rats. OVX rats received a single s.c. injection of vehicle or oestradiol benzoate (OB, 20 μg/rat). This day was designated as day 0. Three or four days later (day 3–day 4), the rats were treated with mifepristone (10 mg/kg) or with two doses of progesterone antiserum and blood samples were obtained at 13.00 and 18.00 h. OB treatment of OVX rats reduced serum LH at 13.00 h and 18.00 h on day 3 but only at 13.00 h on day 4. The administration of mifepristone at 08.00 h to OVX and oestrogen-treated rats induced a significant increase in serum LH at 18.00 h on days 3 and 4, without modifying the values at 13.00 h. When mifepristone was given at 13.00 h a much larger increase in serum LH was obtained at 18.00 h. In OVX and oestrogen-treated rats, adrenalectomy on day 2 (08.00–09.00 h) induced an increase in serum LH at 18.00 h similar to that observed in the OVX and oestrogen-primed rats after mifepristone treatment. In order to determine the specificity of the effect of mifepristone, a group of OVX and oestrogentreated rats was injected with progesterone antiserum at 08.00 and 13.00 h on day 3. Serum LH concentrations at 13.00 and 18.00 h on day 3 were similar to values obtained in OVX rats treated with oestrogen and mifepristone. Serum progesterone was measured at 08.00 and 13.00 h in OVX and OVX and oestrogenprimed rats. At both times, values were similar in OVX rats but oestrogen treatment significantly increased serum progesterone levels. The important role of adrenal progesterone on the regulation of LH secretion in OVX and oestrogen-primed rats is evident from these results. Blocking progesterone action at the receptor level, we showed that OB significantly increased LH values at 18.00 h. On the basis of these studies it is tempting to speculate on the possibility of an inhibitory or stimulatory effect of oestrogen on serum LH concentration in OVX rats, according to the presence or absence of adrenal progesterone action. Journal of Endocrinology (1993) 139, 253–258

scholarly journals Oxytocin Action at the Lactotroph Is Required for Prolactin Surges in Cervically Stimulated Ovariectomized Rats

Endocrinology ◽  
2007 ◽  
Vol 148 (10) ◽  
pp. 4649-4657 ◽  
Author(s):  
De’Nise T. McKee ◽  
Maristela O. Poletini ◽  
Richard Bertram ◽  
Marc E. Freeman
Keyword(s):  
Neuronal Activity ◽  
Dopaminergic Neurons ◽  
Bolus Injection ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Before And After ◽  
Low Levels ◽  
Cervical Stimulation ◽  
Oxytocin Antagonist ◽  
The Mathematical Model

Cervical stimulation induces two daily rhythmic prolactin surges, nocturnal and diurnal, which persist for several days. We have shown that a bolus injection of oxytocin initiates a similar prolactin rhythm, which persists despite low levels of oxytocin after injection. This suggests that oxytocin may trigger the cervical stimulation-induced rhythmic prolactin surges. To investigate this hypothesis, we infused an oxytocin antagonist that does not cross the blood-brain barrier for 24 h before and after cervical stimulation and measured serum prolactin. We also measured dopaminergic neuronal activity because mathematical modeling predicted that this activity would be low in the presence of the oxytocin antagonist. We thus tested this hypothesis by measuring dopaminergic neuronal activity in the tuberoinfundibular, periventricular hypophyseal, and tuberohypophyseal dopaminergic neurons. Infusion of oxytocin antagonist before cervical stimulation abolished prolactin surges, and infusion of oxytocin antagonist after cervical stimulation abolished the diurnal and significantly decreased the nocturnal surges of prolactin. The rhythmic prolactin surges returned after the clearance of the oxytocin antagonist. Hypothalamic dopaminergic activity was elevated in antiphase with prolactin surges, and the antiphase elevation was abolished by the oxytocin antagonist in the tuberoinfundibular and tuberohypophyseal dopaminergic neurons, consistent with the mathematical model. These findings suggest that oxytocin is a physiologically relevant prolactin-releasing factor. However, the cervical stimulation-induced prolactin surges are maintained even in the absence of oxytocin actions at the lactotroph, which strongly suggests the maintenance of prolactin surges are not dependent upon oxytocin actions at the pituitary gland.

Dissociation between the ovarian factors controlling sexual receptivity and preovulatory secretion of LH in cyclic female rats

1987 ◽  
Vol 112 (1) ◽  
pp. 133-138 ◽  
Author(s):  
P. Södersten ◽  
P. Eneroth
Keyword(s):  
Sexual Behaviour ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Sexual Receptivity ◽  
Serum Progesterone ◽  
Lh Surge ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion ◽  
Intact Rats

ABSTRACT Ovariectomy and treatment with oestradiol benzoate (10 μg OB) on the day before behavioural oestrus eliminated the preovulatory surge of LH and reduced the level of sexual receptivity on the following day. Sexual behaviour, but not the LH surge, was restored by progesterone (0·5 mg) given 18 h later. Injection of OB on the day after behavioural oestrus induced a small release of LH and normal sexual behaviour on the following day. Ovariectomy on the day after behavioural oestrus reduced the stimulatory effect of OB on sexual behaviour and eliminated its weakly stimulatory effect on LH release. Sexual behaviour, but not the small LH surge, was restored in these animals by progesterone (0·5 mg) given 18 h later. Treatment of rats ovariectomized 2 days before the day of the LH surge with implants containing oestradiol or injections of oestradiol (1 μg) induced LH surges but the amplitudes of these LH surges were much smaller than those of the normal LH surge. Treatment of intact rats with OB increased serum progesterone levels 24 h later, an effect which was eliminated by ovariectomy. Injections of LH (20 μg) into intact rats on the day after behavioural oestrus also increased serum progesterone concentrations but failed to stimulate sexual behaviour. It is suggested that OB treatment of intact rats on the day after behavioural oestrus stimulates sexual behaviour by inducing a surge of LH secretion which activates ovarian secretion of progesterone. Thus, oestrogen and progesterone but not the LH surge are essential for sexual behaviour. Whereas oestradiol and progesterone restore normal sexual behaviour in ovariectomized rats, additional ovarian factors may be required for induction of normal LH surges. J. Endocr. (1987) 112, 133–138

Inhibition of sexual behaviour in lactating rats

1983 ◽  
Vol 99 (2) ◽  
pp. 189-197 ◽  
Author(s):  
P. Södersten ◽  
S. Hansen ◽  
P. Eneroth
Keyword(s):  
Dopamine Receptor ◽  
Sexual Behaviour ◽  
Inhibitory Effect ◽  
Daily Treatment ◽  
Female Rats ◽  
Serum Prolactin ◽  
Dopamine Receptor Agonist ◽  
Serum Progesterone ◽  
Behavioural Effects

Treatment with oestradiol benzoate (OB; 2–250 μg) and progesterone (0·5–25 mg) failed to induce sexual behaviour in lactating rats 6 days after parturition. Removal of pups permitted the induction of sexual behaviour by OB and progesterone and the inhibitory effect of the presence of pups was proportional to the number present. Ovariectomy of lactating rats or reduction of serum prolactin levels in intact lactating rats by daily treatment with the dopamine receptor agonist bromocriptine (0·5 mg/day) permitted the induction of sexual behaviour despite the presence of suckling pups. Removal of pups from lactating rats and subsequent maintenance of high prolactin levels by daily treatment with the dopamine receptor antagonist domperidone (2·5 mg/day) maintained the state of refractoriness to the behavioural effects of OB and progesterone provided that the ovaries remained in situ. Inhibition of sexual behaviour in lactating rats could be maintained after ovariectomy by implantation of progesterone-filled, but not androgen-filled implants at the time of ovariectomy. Removal of the pups or reduction of prolactin levels by bromocriptine treatment permitted the induction of sexual behaviour by OB in ovariectomized progesterone-implanted lactating rats. Inhibition of the behaviour in ovariectomized progesterone-implanted lactating rats could be maintained after pup removal by daily domperidone treatment. Continuously raised serum progesterone or prolactin levels have no effect on the induction of sexual behaviour in female rats but the present data suggest that during lactation progesterone and prolactin act in synergy to inhibit the behaviour.

Evidence that prolactin does not affect the induction of sexual behaviour by oestradiol and progesterone in ovariectomized rats

1983 ◽  
Vol 99 (2) ◽  
pp. 181-187 ◽  
Author(s):  
P. Södersten ◽  
S. Hansen ◽  
P. Eneroth
Keyword(s):  
Receptor Antagonist ◽  
Dopamine Receptor ◽  
Sexual Behaviour ◽  
Inhibitory Effect ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Behavioural Effect ◽  
Dopamine Receptor Antagonist ◽  
Oestradiol Benzoate ◽  
Acute Increase

Injection of 2·5 mg of the dopamine receptor antagonist domperidone raised serum prolactin concentrations within 3 h and high prolactin levels were maintained for 12 h in ovariectomized rats pretreated with 2 μg oestradiol benzoate (OB). This dose of domperidone stimulated the display of sexual behaviour in ovariectomized OB-treated rats within 3 h of administration. The behavioural effect of domperidone, but not its effect on serum prolactin concentrations, was blocked by adrenalectomy. Daily treatment with domperidone had no inhibitory effect on the subsequent induction of sexual behaviour by OB and progesterone in ovariectomized rats. A slight facilitation of the behaviour was noticed in OB-treated rats given daily domperidone injections, but this effect was cancelled by adrenalectomy. The results suggest that an acute increase in serum prolactin levels has no effect on the induction of sexual behaviour by OB in itself, but can stimulate the secretion of an adrenal product, perhaps progesterone, which facilitates the behaviour. Similarly, constant high levels of prolactin by themselves have no effect on the subsequent induction of sexual behaviour by OB and progesterone.

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

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.

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