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ABSTRACT
The concentrations of oestradiol and oestrone in peripheral plasma of male and female ferrets 5 days before and 7, 15 and 30 days after birth were measured. Both steroids were present in high concentrations prenatally. Much lower levels were found in samples collected on day 7 and later, when the concentrations were similar to those of adult gonadectomized animals. No significant sex difference was seen for the concentration of either steroid at any age studied. These results, and those previously reported showing the absence of a circulating binding protein and the presence of oestradiol receptors in the hypothalamus in the perinatal period in this species, suggest that brains of both males and females are exposed to significant amounts of oestrogen during development. These findings lend support to the possibility that prenatal exposure to oestrogen plays a role in organizing the potential for female behaviour in male and female ferrets.
J. Endocr. (1984) 100, 161–166
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ABSTRACT
Six experiments were carried out to determine whether dihydrotestosterone (5α-androstan-17β-ol-3-one; DHT) acts to inhibit oestradiol (OE2)-induced lordosis behaviour after its metabolic conversion to 5α-androstane-3α,17β-diol (3α-androstanediol, 3α-Adiol). In experiments 1 and 2, ovariectomized rats were treated with several doses of DHT or 3α-Adiol, injected with OE2 and progesterone, and tested for lordosis responsiveness. Significant inhibition of lordosis occurred after a dose of 3α-Adiol which was approximately threefold less than the effective DHT dose. In experiments 3 and 4, plasma concentrations of DHT and 3α-Adiol were measured after the injection of these steroids to ovariectomized rats at doses shown to be both sufficient or insufficient to inhibit lordosis. Behaviourally effective dosages of DHT and 3α-Adiol produced circulating concentrations of 3α-Adiol greater than those produced by behaviourally ineffective doses of DHT or 3α-Adiol. At 30 min after injection of DHT (experiment 3), 78·8% of plasma androgens were in the form of 3α-Adiol, while after injection of 3α-Adiol, only 7·4% were DHT. When plasma DHT and 3α-Adiol were measured at 3, 6, 9 and 12 h after steroid injection (experiment 4), plasma levels of 3α-Adiol produced by the behaviourally subthreshold dose of DHT were significantly lower than levels produced by behaviourally sufficient dosages of DHT or 3α-Adiol. In experiments 5 and 6, concentrations of DHT and 3α-Adiol were measured in five brain regions 1 and 6 h after injection of behaviourally sufficient doses of these steroids to ovariectomized females. At 1 h after injection, similar levels of DHT and 3α-Adiol were measured in DHT- and 3α-Adiol-injected females, and DHT concentrations in the preoptic area were significantly higher in both groups than in any other brain area. At 6 h, animals injected with DHT had significantly higher levels of DHT in all brain areas combined than did 3α-Adiol-or vehicle-injected animals. Brain concentrations of 3α-Adiol were not different between groups injected with DHT, 3α-Adiol or vehicle at this time. In brain, 34·6% of DHT had been converted to 3α-Adiol after 1 h and 53·0% of 3α-Adiol had been converted to DHT. These results suggest that the inhibitory action of DHT on lordosis may be a consequence of its conversion to 3α-Adiol, and that this conversion may account for the higher behavioural potency of the latter steroid.
Journal of Endocrinology (1992) 134, 183–195
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ABSTRACT
Administration of the synthetic steroid, 17β-hydroxy-17α-methyl-estra-4,9,11-triene-3-one (methyltrienolone, R1881), which is an androgen receptor agonist not metabolized in vivo, at doses of 400, 800 or 2400 μg/kg s.c. in propylene glycol stimulated mounting and ejaculation only slightly in sexually experienced castrated rats. A similar low level of mating was observed in a group of castrated rats given testosterone at doses of 400 followed by 800 μg/kg. However, when treated with a higher dose of testosterone (2400 μg/kg) these castrated rats displayed significantly higher levels of mounting and ejaculation than rats treated with any of the doses of R1881. Also, when this higher dosage of testosterone was substituted for each dose of R1881, significant increments in mounting and ejaculation occurred in all groups. These findings show that R1881 is only marginally effective in restoring sexual behaviour in castrated rats, suggesting that the activation of neural androgen receptors cannot by itself account for the activational effect of testosterone on mating behaviour in gonadally intact male rats.
J. Endocr. (1987) 113,15–20
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Gonadectomized rats bearing s.c. Silastic capsules containing crystalline oestradiol-17β diluted with cholesterol, or oestradiol-17β dissolved in sesame oil were tested for the presence of a diurnal rhythm in the display of lordotic behaviour. In experiment 1, female rats received four consecutive tests at intervals of 8 h in a lighting regimen of 12 h light: 12 h darkness beginning 4, 14 and 28 days after implantation of 5 mm capsules of oestradiol. After a single test on day 4, male rats were tested on days 14–15 only, at the same times as the female rats. Female animals were tested while vaginal–cervical stimulation was prevented by vaginal masking beginning 35 days after implantation of oestradiol. In experiment 2, lordotic responsiveness of female rats was assessed beginning 4 days after implantation of oestradiol once on each of 3 consecutive days, with each test occurring at a different time of day. Finally, in experiment 3, female rats were tested as in experiment 1 beginning 4 days after implantation of lower threshold amounts of oestradiol in oil-filled capsules. In no experiment were changes in lordotic behaviour observed as a function of the time of day. These findings failed to support recent reports of a sexually dimorphic rhythm in lordotic responsiveness to oestradiol in the rat.
