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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
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ABSTRACT
Male rats showed maternal behaviour within 72 h after the onset of continuous exposure to newborn rat pups. The latency of the behavioural response could be reduced by daily treatment with the dopamine receptor antagonist domperidone (2 × 2·5 mg/rat), which increased serum prolactin concentrations (241·4 ± 26·5 (s.e.m.) μg/l) above those of vehicle-treated males exposed to pups (25·3 ± 11·7 μg/l). Male rats did not respond to exposure to pups by secreting prolactin; keeping endogenous prolactin concentrations at a minimum (2·8±0·1 μg/l) by daily treatment with the dopamine receptor agonist bromocriptine (0·5 mg/rat) did not affect the behavioural response of male rats to newborn pups. Neither exposure to pups nor the modest hyperprolactinaemia induced by daily domperidone treatment affected the display of male sexual behaviour by male rats.
J. Endocr. (1984) 102, 115–119
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ABSTRACT
The frequency of pup sucking behaviour was related to serum concentrations of prolactin and LH in rats during various phases of lactation. Sucking frequency and prolactin levels decreased and LH levels increased as lactation progressed. There was no clear relationship between sucking frequency and either prolactin or LH levels. Serum prolactin concentrations were highest when the rats spent most of their time away from their pups and lowest when the rats spent most of their time with the pups attached to their nipples. Prolactin was secreted episodically during prolonged continuous nipple stimulation. Removal of the pups in late lactation and replacement with a newborn litter increased sucking frequency but did not affect serum LH levels and only marginally increased serum prolactin levels. Injection of the dopamine receptor antagonist domperidone produced a far more pronounced release of prolactin from the pituitary gland in early than in late lactation. A circadian control mechanism and an episodic pattern of release may contribute to the great variation in serum prolactin concentrations seen in early lactation; decreased pituitary sensitivity to dopamine receptor blockade may be related to the low concentration of serum prolactin found in late lactation.
J. Endocr. (1984) 102, 251–256
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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.
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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.
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Male rats were given daily injections of the antioestrogen ethamoxytriphetol (MER-25, 100 μ/day) or oil during the first 10 days of life. Rats treated with MER-25 showed a more pronounced diurnal rhythm in both mounting behaviour and lordosis behaviour than did oil-treated rats when tested as intact adults and after castration together with treatment with testosterone- or oestradiol-filled constant release implants. Serum levels of androgen varied markedly in samples obtained at four different times of the light: darkness (LD) cycle in both neonatal treatment groups and no significant LD-dependent pattern was obvious. Castration and treatment with testosterone implants produced stable androgen levels which showed little individual variation and did not vary with the LD cycle. The results supported the hypothesis that perinatal androgen stimulation affects the development of sexual behaviour in rats primarily by decreasing the diurnal rhythmicity of the behaviour of the adult.
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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
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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
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ABSTRACT
The time-interval between parturition and the display of sexual receptivity varied between 13·5 ± 0·7 and 35·9 ± 2·5 days in rats with litters of between 1 and 24 pups. Body weight gain decreased and the avidity of pup sucking behaviour, measured by the latency before the pups, placed on the ventrum of an anaesthetized mother, attached to a nipple of the mother, increased as litter size increased. Litter-shifting procedures, which introduced asynchrony between the lactational age of the mother and the age of the pups, produced deficiencies in sucking behaviour and did not prolong the time-interval between parturition and the display of sexual receptivity by the mother. By keeping the lactational age of the mother in synchrony with the age of the pups and depriving the pups of maternal contact and nutrition every alternate day, the time-interval between parturition and the display of sexual receptivity by the mother was prolonged by 17 days, the avidity of pup sucking behaviour markedly enhanced and the body weight gain of the pups retarded in comparison with mothers and pups continuously living together. The results show that the display of the first postlactational behavioural oestrus and surge of pituitary LH secretion can be greatly delayed by an increase in the avidity of pup sucking behaviour.
J. Endocr. (1985) 104, 419–425
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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.
