Naloxone stimulates sexual behaviour in lactating rats

1987 ◽  
Vol 113 (3) ◽  
pp. 423-427 ◽  
Author(s):  
G. Forsberg ◽  
P. Eneroth ◽  
P. Södersten

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

1987 ◽  
Vol 113 (3) ◽  
pp. 429-434 ◽  
Author(s):  
G. Forsberg ◽  
I. Bednar ◽  
P. Eneroth ◽  
P. Södersten

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


1983 ◽  
Vol 99 (2) ◽  
pp. 181-187 ◽  
Author(s):  
P. Södersten ◽  
S. Hansen ◽  
P. Eneroth

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.


1987 ◽  
Vol 112 (1) ◽  
pp. 133-138 ◽  
Author(s):  
P. Södersten ◽  
P. Eneroth

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


1985 ◽  
Vol 106 (2) ◽  
pp. 183-188 ◽  
Author(s):  
G. Forsberg ◽  
P. Södersten ◽  
P. Eneroth

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


1993 ◽  
Vol 139 (2) ◽  
pp. 253-258 ◽  
Author(s):  
A. M. Salicioni ◽  
R. W. Carón ◽  
R. P. Deis

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


1979 ◽  
Vol 80 (3) ◽  
pp. 389-395 ◽  
Author(s):  
P. SÖDERSTEN ◽  
S. HANSEN

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.


Analgesia ◽  
1999 ◽  
Vol 4 (1) ◽  
pp. 27-32 ◽  
Author(s):  
John S. Partilla ◽  
F. Ivy Carrol ◽  
James B. Thomas ◽  
Kenner C. Rice ◽  
Dennis M. Zimmerman ◽  
...  

2021 ◽  
pp. 174207
Author(s):  
Atsuo Tahara ◽  
Hajime Takamatsu ◽  
Akiyoshi Ohtake ◽  
Keiko Tanaka-Amino ◽  
Seiji Kaku

1983 ◽  
Vol 98 (1) ◽  
pp. 7-17 ◽  
Author(s):  
R. F. Walker

In ovariectomized rats treated chronically with oestrogen there is a loss of positive feedback effects on LH secretion. This was not due to depletion of pituitary LH since injection of LH releasing hormone (LH-RH; 50 ng/100 g body wt) caused a significant (P < 0·01) rise in serum LH even after the loss of spontaneous LH surges. However, the magnitude of the increase in serum LH in response to LH-RH was greater (412 ± 41 μg/l) before than after (291 ± 29 μg/l) loss of the LH surges. Excessive blood sampling was also not responsible, since positive feedback responses declined comparably in rats bled daily or once every 3–4 days. Progesterone (0·5 mg s.c.), administered for 5 consecutive days, failed to restore LH surges indicating that deficiency of this steroid after ovariectomy does not cause positive feedback responses to disappear in rats exposed chronically to oestrogen. Moreover regular daily fluctuations in serum progesterone, probably of adrenal origin, occurred before as well as after daily LH surges were lost. Serotonin content and turnover were depressed (P < 0·05) when ovariectomized rats first received the subcutaneous capsules containing oestrogen. This change correlated temporally with the onset of daily LH surges and was eventually lost. After 30 days exposure to oestrogen, serotonin turnover increased (P < 0·01) and positive feedback responses were absent. Catecholamine levels and turnover did not show differential responses to oestrogen and were depressed after acute as well as chronic steroid treatment. p-Chlorophenylalanine (pCPA; 250 mg/kg)+ l-dihydroxyphenylalanine (l-DOPA; 200 mg/kg), which depress serotonin and enhance catecholamine synthesis respectively, failed to reinstate LH surges, but these were restored in 22% of the rats receiving l-DOPA alone. pCPA, followed 2 days later by 5-hydroxytryptophan (5-HTP) at 11.00 h, reinstated LH surges in 88% of rats, and a dose–response curve showed that as little as 4 mg 5-HTP/kg stimulated repetitive LH surges when given with pCPA according to this schedule. However, the administration of α-methyl-p-tyrosine + l-DOPA, an analogous treatment involving catecholamines, was only marginally effective (15%). These findings suggest that perturbations of monoamine metabolism occurring in ovariectomized rats exposed to oestrogen for several weeks contribute to loss of daily LH surges. Since pCPA + 5-HTP restored LH surges most effectively, then positive feedback may disappear as the facilitatory effect of serotonin is lost after chronic oestrogen administration.


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