INDUCTION OF SEXUAL RECEPTIVITY IN OVARIECTOMIZED RATS BY PULSE ADMINISTRATION OF OESTRADIOL-17β

1981 ◽  
Vol 89 (1) ◽  
pp. 55-62 ◽  
Author(s):  
P. SÖDERSTEN ◽  
P. ENEROTH ◽  
S. HANSEN
Keyword(s):  
Single Injection ◽  
Serum Levels ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Sexual Receptivity ◽  
Behavioural Responses ◽  
Time Points ◽  
Progesterone Treatment ◽  
Oestradiol Benzoate ◽  
Stimulation Of

Constant-release implants filled with oestradiol-17β induced sexual receptivity in ovariectomized rats in response to progesterone treatment if they were implanted 32 h before behavioural testing. A 20 h period of exposure to oestradiol, by implantation 32 h before testing and removal of the implants 20 h later, was sufficient for induction of the behaviour. The exposure time necessary for behavioural responses could be further reduced to two 4 h periods, between 32 and 28 h and between 16 and 12 h, before testing. Serum levels of oestradiol were raised within 1 h of oestradiol implantation and declined rapidly after implant removal. A single injection of oestradiol benzoate was much more potent than a single injection of oestradiol in inducing sexual receptivity in ovariectomized rats, but this difference in potency was reversed if two appropriately timed injections were given. Oestrone- or oestriol-filled implants were relatively ineffective in inducing sexual receptivity. It is suggested that oestradiol has to be present at crucial time points to prepare an ovariectomized rat to respond behaviourally to progesterone treatment and that oestradiol is the principal oestrogen in the stimulation of sexual behaviour in female rats.

INDUCTION OF SEXUAL RECEPTIVITY BY OESTRADIOL BENZOATE IN CYCLIC FEMALE RATS: INFLUENCE OF OVARIAN SECRETIONS BEFORE INJECTION OF OESTRADIOL BENZOATE

1979 ◽  
Vol 80 (3) ◽  
pp. 389-395 ◽  
Author(s):  
P. SÖDERSTEN ◽  
S. HANSEN
Keyword(s):  
Sexual Behaviour ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Sexual Receptivity ◽  
Behavioural Effect ◽  
Progesterone Treatment ◽  
Oestradiol Benzoate

The ability of cyclic female rats to show sexual receptivity 24 h after an injection of 2 μg oestradiol benzoate (OB) was lost 24 h after ovariectomy. Exposure of cyclic rats to anti-oestrogen (nitromophene monocitrate) implants 24 h before ovariectomy and OB treatment prevented the latter from inducing sexual receptivity within 24 h of administration. Treatment of ovariectomized rats with constant release implants filled with an oil solution of 15 μg oestradiol/ml had no behavioural effect in itself, but prepared the rats to show lordosis 24 h after administration of OB. Progesterone treatment (4 mg) induced sexual behaviour in cyclic rats on days other than that of the oestrous cycle when the rats are normally receptive. Evidence is presented that a lower level of oestradiol stimulation than that present during pro-oestrus was needed for the induction of sexual receptivity in ovariectomized rats. It is suggested that the low basal level of oestradiol which was present throughout the oestrous cycle was necessary for the induction of sexual receptivity and that an increase in oestradiol stimulation served to increase the behavioural sensitivity to progesterone.

EFFECTS OF OESTRADIOL AND PROGESTERONE ON THE INDUCTION AND DURATION OF SEXUAL RECEPTIVITY IN CYCLIC FEMALE RATS

1977 ◽  
Vol 74 (3) ◽  
pp. 477-485 ◽  
Author(s):  
P. SÖDERSTEN ◽  
S. HANSEN
Keyword(s):  
Behavioural Response ◽  
Female Rats ◽  
Sexual Receptivity ◽  
Repeated Treatment ◽  
Progesterone Treatment ◽  
Oestradiol Benzoate

SUMMARY Intact 4-day cyclic rats showed sexual receptivity 24 h after an injection of oestradiol benzoate (OB) on any day of the cycle except on the second day after the display of spontaneous oestrus. Ovariectomy at the time of OB treatment abolished the behavioural response, but receptivity was restored by progesterone. Progesterone treatment early on the day of behavioural oestrus advanced the display of receptivity but did not affect the time at which oestrus ended. Repeated treatment of sexually receptive rats with progesterone did not affect the duration of oestrus. These results show that sexual receptivity in the intact rat cannot occur in the absence of oestradiol and progesterone. The results further suggest that progesterone may not be associated with the mechanisms terminating behavioural oestrus in rats. Treatment with OB on the day of oestrus can prolong the duration of receptivity but only at a higher dosage than that needed for induction of receptivity.

SENSITIVITY OF ANTERIOR HYPOTHALAMIC AREAS TO GONADAL STEROID IMPLANTATION IN ANDROGENIZED FEMALE RATS

1977 ◽  
Vol 74 (2) ◽  
pp. 315-NP ◽  
Author(s):  
A. DANGUY ◽  
J. L. PASTEELS ◽  
F. ECTORS
Keyword(s):  
Single Injection ◽  
Mammary Glands ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Male Rats ◽  
Control Synthesis ◽  
Normal Female ◽  
Immunofluorescence Studies ◽  
Oestradiol Benzoate ◽  
Stimulation Of

A single injection of 1 mg of a complex of testosterone esters on day 5 of life was used to prepare constantly oestrous rats. Such androgenized female rats were then ovariectomized and submitted to stereotaxical implantation of 1 μg oestradiol benzoate, 5 μg testosterone isobutyrate or, as a control, 10 μg cholesterol in the anterior hypothalamic areas. The effects of the steroids on plasma and pituitary FSH and LH were assessed by radioimmunoassay. As reported previously by us in normal female and male rats, the preoptic–suprachiasmatic area (POA) was able to control synthesis and secretion of both gonadotrophins and did not lose its sensitivity to oestradiol and testosterone in androgenized rats. Evidence for enhanced prolactin secretion in androgenized rats was derived from immunofluorescence studies of the pituitary gland and from histology of the mammary glands. In this respect the condition of the androgenized females was opposite to that of the males. The present work demonstrated that stimulation of prolactin secretion in androgenized female rats resulted from oestrogen action due to permanent oestrus rather than from impairment of hypothalamo-hypophysial relationships. Indeed, prolactin stimulation was suppressed when the androgenized rats were ovariectomized and restored when they were subsequently implanted with oestradiol in the POA.

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

Naloxone reverses post-ejaculatory inhibition of sexual behaviour in female rats

1987 ◽  
Vol 113 (3) ◽  
pp. 429-434 ◽  
Author(s):  
G. Forsberg ◽  
I. Bednar ◽  
P. Eneroth ◽  
P. Södersten
Keyword(s):  
Sexual Behaviour ◽  
Opioid Peptide ◽  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Sexual Receptivity ◽  
Peptide Receptor ◽  
Oestradiol Benzoate ◽  
Brain And Spinal Cord ◽  
The Brain

ABSTRACT Sexual receptivity was inhibited in ovariectomized rats treated with oestradiol benzoate (OB: two injections of 2 μg) and progesterone (0·5 mg) immediately after ejaculation by the male and restored after the end of the post-ejaculatory refractory period in the male. The post-ejaculatory inhibition of sexual receptivity was reversed by i.p. (5 mg), intracerebroventricular (50 μg) or intrathecal (50 μg) injection of the opioid peptide receptor antagonist naloxone. The concentration of serum β-endorphin-like immunoreactivity in ovariectomized rats treated with OB plus progesterone was unaltered by sexual interactions with males (18·3 ± 6·0 (s.e.m.), 26·4 ± 2·1 and 21·8 ± 6·1 pmol/l before sexual activity, after ejaculation and after the end of the post-ejaculatory interval) but reduced to non-detectable by hypophysectomy. Subcutaneous injection of 10 μg β-endorphin raised serum concentrations of β-endorphin-like immunoreactivity but did not affect the display of sexual behaviour. The behaviour was also unaffected by intracerebroventricular injection of 0·1, 0·2 or 1·0 μg β-endorphin or by injections of 0·25 μg β-endorphin in the periaqueductal central grey of the mesencephalon. The results show that ejaculation by male rats causes a transient inhibition of sexual receptivity in the female which may be dependent upon opioid peptide receptor mechanisms in the brain and spinal cord. It is unlikely that the peptide is β-endorphin. J. Endocr. (1987) 113, 429–434

EVIDENCE THAT PROGESTERONE DOES NOT INHIBIT THE INDUCTION OF SEXUAL RECEPTIVITY BY OESTRADIOL-17β IN THE RAT

1981 ◽  
Vol 89 (1) ◽  
pp. 63-69 ◽  
Author(s):  
P. SÖDERSTEN ◽  
P. ENEROTH
Keyword(s):  
Serum Levels ◽  
Behavioural Response ◽  
Oestrous Cycle ◽  
Implant Removal ◽  
Ovariectomized Rats ◽  
Sexual Receptivity ◽  
Behavioural Effect ◽  
Inhibitory Role ◽  
Progesterone Treatment

Progesterone-filled constant-release implants facilitated the induction of sexual receptivity in ovariectomized rats given implants of oestradiol-17β precisely 32 h before testing, irrespective of the time of implantation. Inhibition by progesterone implants of the behavioural response to an injection of progesterone occurred after the facilitation 32 h after oestradiol implantation. Sexual receptivity could be induced in pseudopregnant rats in the absence of progesterone treatment by injection of 1 μg oestradiol 32 and 16 h before testing at a time when endogenous serum levels of oestradiol were low and progesterone levels were high. The behavioural response of ovariectomized rats implanted with oestradiol and tested daily was unaffected by implantation of progesterone at the time of oestradiol implantation, although serum levels of progesterone varied with the number of progesterone implants inserted. Inhibition by progesterone implants of the behavioural response to an injection of progesterone 6 h before behavioural testing occurred only if the progesterone implants were present for at least 32 h of a 48 h period. Serum levels of progesterone were raised within 1 h of progesterone implantation and declined within a 6 h period after implant removal. It is concluded that progesterone does not inhibit the behavioural effect of oestradiol and that progesterone does not play an inhibitory role in the regulation of the behavioural oestrous cycle in our strain of rats.

EFFECT OF OVARIAN STEROIDS ON PREPUTIAL GLAND ODOURS IN THE FEMALE RAT

1978 ◽  
Vol 77 (3) ◽  
pp. 397-403 ◽  
Author(s):  
A. J. THODY ◽  
H. DIJKSTRA
Keyword(s):  
Single Injection ◽  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Whole Body ◽  
Female Rat ◽  
Preputial Gland ◽  
Intact Female ◽  
Oestradiol Benzoate ◽  
Experienced Male

Sexually experienced male rats were used to test for whole body and preputial gland odours of female rats. The male rats clearly preferred whole body odours of intact female rats to those of preputialectomized female rats. The male rats also preferred the odour of preputial gland tissue of intact female rats to that of ovariectomized female rats and were especially attracted to the preputial gland odours of female rats in pro-oestrus and oestrus. The preputial gland odours of ovariectomized rats that had received oestradiol benzoate for 7 days were attractive to male rats, although similar treatment with progesterone was ineffective. However, a single injection of progesterone given 72 h after a single injection of oestradiol benzoate not only made ovariectomized rats receptive, but also made their preputial gland odours attractive to male rats. The results suggest that the preputial gland of the female rat is responsible for odours that serve to attract sexually experienced male rats. Ovarian steroids, as well as controlling receptivity in the female rat, would also appear to control the production of sex attractants in the preputial gland. There was no relationship between the size of the preputial glands and their ability to attract male rats which suggests that preputial gland growth and production of sex attractants are not under the same hormonal control.

SERUM LEVELS OF OESTRADIOL-17β AND PROGESTERONE IN RELATION TO SEXUAL RECEPTIVITY IN INTACT AND OVARIECTOMIZED RATS

1981 ◽  
Vol 89 (1) ◽  
pp. 45-54 ◽  
Author(s):  
P. SÖDERSTEN ◽  
P. ENEROTH
Keyword(s):  
Sexual Behaviour ◽  
Close Correlation ◽  
Serum Levels ◽  
Oestrous Cycle ◽  
Ovariectomized Rats ◽  
Sexual Receptivity ◽  
Behavioural Responses ◽  
Low Serum

Serum levels of oestradiol-17β fluctuated markedly during the oestrous cycle of rats. The onset of sexual receptivity occurred in close correlation with increasing serum levels of progesterone. The serum levels of oestradiol and progesterone in ovariectomized rats implanted with constant-release implants filled with oestradiol or progesterone were related to the amount of hormone in the implants. Constant low serum levels of oestradiol stimulated sexual behaviour in ovariectomized rats, but progesterone stimulation was required for maximum behavioural responses. Peak levels of progesterone in the serum during the oestrous cycle were much higher than those needed for induction of the behaviour in ovariectomized, oestradiol-treated rats. Progesterone, administered in physiological doses, inhibited the induction of sexual receptivity caused by oestradiol and progesterone and the inhibition depended on the strength of the stimulation with oestradiol.

OESTROGEN RESPONSES OF RATS NEONATALLY STERILIZED WITH STEROIDS

1969 ◽  
Vol 45 (3) ◽  
pp. 415-420 ◽  
Author(s):  
T. R. WRENN ◽  
JOAN R. WOOD ◽  
J. BITMAN
Keyword(s):  
Testosterone Propionate ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Uterine Weight ◽  
Oestradiol Benzoate

SUMMARY At 75 days of age, female rats neonatally sterilized with oestradiol benzoate or testosterone propionate were compared with normal and ovariectomized rats with regard to their 6-hr. response to 0·2 μg. oestradiol 17β. The greatest increases in uterine weight, glucose and glycogen concentrations and per cent uterine water occurred in the ovariectomized animals. A marked oestrogen response also occurred in the animals neonatally sterilized with oestradiol benzoate. The response of the normal rats was slight, and the testosterone propionate-treated rats were the least affected. Adrenal, pituitary, and ovarian weights were found to be affected by the neonatal hormone treatments. Vaginal patency was completely inhibited in the rats injected with testosterone propionate. It is concluded that rats neonatally sterilized with steroids are much less suitable than ovariectomized animals for oestrogen assays.

Antioestrogen inhibition of oestradiol-induced alterations in hypothalamic noradrenaline turnover

1985 ◽  
Vol 106 (1) ◽  
pp. 37-42 ◽  
Author(s):  
C. Hiemke ◽  
B. Poetz ◽  
R. Ghraf
Keyword(s):  
Brain Area ◽  
Serum Levels ◽  
Ovariectomized Rats ◽  
Noradrenaline Turnover ◽  
Stimulatory Action ◽  
Enhanced Sensitivity ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Secretory System

ABSTRACT Long-term (4–6 weeks) ovariectomized rats were injected with either oestradiol benzoate (OB; 20 μg s.c.) or monohydroxytamoxifen (MTAM; 0·2 mg i.p.) plus OB. Oestradiol benzoate was administered at 12.00 h on day 0 and MTAM was given immediately before OB, followed by further injections twice daily to maintain sufficiently high antioestrogen levels. When given alone, OB reduced the serum levels of LH during the morning (08.00–09.00 h) and afternoon (17.30–18.30 h) hours of day 3 after priming. The feedback actions of OB on LH release were accompanied by time-dependent alterations of noradrenaline turnover in the preoptic–anterior hypothalamic brain area (POAH). On day 3 after priming the noradrenaline turnover rate was reduced in the morning and increased in the afternoon. The increase correlated with an enhanced sensitivity of the LH secretory system to progesterone. The antioestrogen MTAM blocked the OB-induced sensitization of LH release to the stimulatory action of progesterone and interfered with the stimulatory long-term effect of oestradiol on hypothalamic noradrenaline turnover. The data strongly support the view that the oestrogen-induced afternoon increase of noradrenaline turnover in the POAH represents a pre-requisite for the induction of LH surges. The stimulatory effect of oestradiol on hypothalamic noradrenaline turnover seems to be mediated by a classical oestrogen receptor mechanism. J. Endocr. (1985) 106, 37–42

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