Search Results

You are looking at 1 - 8 of 8 items for

  • Author: R. F. Parrott x
Clear All Modify Search
Restricted access

R. F. Parrott

ABSTRACT

Ten adult prepubertally castrated rams were injected with 5α-dihydrotestosterone propionate (DHTP; 20 mg/day) for 3 weeks to stimulate genital development. Thereafter, half of the sheep were injected with testosterone (100 mg/day) for a further 4 weeks, while the remainder received the same dose of 17β-hydroxy-17α-methyl-estra-4,9,11-triene-3-one (methyltrienolone; R1881). All the animals were tested for sexual behaviour on 15 occasions with ovariectomized ewes in which oestrous behaviour was induced by injections of 50 μg oestradiol-17β benzoate at 4- to 5-day intervals. Behavioural tests were of 10 min duration and were carried out thrice weekly over a 5-week period, starting in the final week of DHTP treatment. Animals treated with testosterone showed a highly significant increase in courtship behaviour (tongue-flicks; lunges and nudges) after only four daily injections and this level of activity was maintained to the end of the experiment. However, the incidence of courtship activity in sheep treated with R1881 was similar to that recorded during the period of DHTP treatment. All animals given testosterone displayed mounts with pelvic thrusts and erections, and achieved intromission with ejaculation. These activities remained significantly more frequent than in sheep treated with R1881, starting from tests 9, 8 and 12 respectively. Four of the five individuals in the group given R1881 showed occasional mounts with thrusts, three showed sporadic erections and one sheep intromitted in the final test. These results indicate that, in contrast to the rat, R1881 has only very weak effects on sexual behaviour in the castrated ram.

J. Endocr. (1986) 110, 481–487

Restricted access

R. F. PARROTT

SUMMARY

The ability of 19-hydroxytestosterone propionate (150 μg/day) to maintain sexual behaviour, accessory organ weights and the number of penile spines in experienced adult male rats in the 5 weeks after castration was compared with intact males and castrated animals receiving testosterone propionate (75 μg/day) or oil treatment. In a second experiment a group of male rats receiving dihydrotestosterone propionate (150 μg/day) was also included. 19-Hydroxytestosterone did not maintain ejaculatory performance but animals that ejaculated had refractory periods similar to those in intact and testosterone-treated groups. Dihydrotestosterone, however, slowed the rate of decline of ejaculatory performance but the refractory periods were comparable to those in castrated controls. The former action of dihydrotestosterone was attributed to its stimulatory effect on peripheral structures, especially the penile spines. 19-Hydroxytestosterone was shown to have no peripheral effect at doses up to 1800 μg every other day. The results are discussed in terms of a theory of testosterone action involving aromatization in the brain and 5α-reduction peripherally.

Restricted access

R. F. PARROTT

Department of Physiology, Royal Veterinary College, London, NW1 OTU

(Received 11 November 1974)

Castration in the rat causes an increase in the post-ejaculatory refractory period, often before ejaculation declines. This indicates a central effect of androgen withdrawal and can be prevented only by treatment with aromatizable androgens (Parrott, 1975), suggesting that the effect involves conversion of androgen to oestrogen. In support of this suggestion, two androgen/oestrogen intermediates, 19-hydroxytestosterone (Parrott, 1974) and 19-hydroxyandrostenedione (Parrott, 1975), and oestrogen (Davidson, 1969; Parrott, 1975) maintain normal refractory periods in castrated rats. This report describes the behavioural action of 19-nortestosterone, an androgen without a 19-methyl group. Some androgens induce receptivity in ovariectomized rats when combined with progesterone. This effect is inhibited by antioestrogens (Whalen, Battie & Luttge, 1972), implicating the involvement of aromatization. Because of this, 19-nortestosterone was first studied in female rats.

In week 1, 22 ovariectomized Sprague-Dawley (MRC) rats received 10 μg oestradiol benzoate

Restricted access

R. F. PARROTT and F. HILLS

SUMMARY

Prolactin concentrations were measured in serum from wethers at various times of the year before and during treatment with testosterone propionate, dihydrotestosterone propionate, 19-hydroxytestosterone dipropionate and oestradiol dipropionate. Levels of prolactin in serum were lower in untreated wethers during short (October) than during long (April–August) days. Seasonal differences persisted throughout the experiment but became less obvious during treatment with oestradiol dipropionate and 19-hydroxytestosterone dipropionate, both of which raised prolactin concentrations. Neither testosterone propionate nor dihydrotestosterone propionate altered the levels of prolactin.

Restricted access

R. F. PARROTT and J. E. BOOTH

Department of Physiology, Royal Veterinary College, London, NW1 OTU

(Received 21 August 1975)

19-Hydroxytestosterone (17β-hydroxy-4-androsten-19-ol-3-one; 19HT) and its 5α-reduced metabolite (17β-hydroxy-5α-androstan-19-ol-3-one; 5α-19HT)have negligible stimulatory effects on androgen target organs in the castrated rat (Parrott, 1974, 1975). The object of this study was to establish whether these androgens can limit the release of luteinizing hormone (LH) from the pituitary. To investigate this they were compared with testosterone for their ability to prevent compensatory ovarian hypertrophy in the unilaterally ovariectomized rat.

Forty-eight adult female Sprague-Dawley (MRC) rats were hemi-ovariectomized and allocated to six groups of eight animals each. Body weights and the weight of the left ovary were recorded. Starting from ovariectomy, rats received ten daily 0·2 ml s.c. injections after which they were killed. Treatments were oil vehicle (control); testosterone, 1 mg/day; 19HT, 1 mg/day; 19HT, 2 mg/day; 5α-19HT, 1 mg/day; 5α-19HT, 2 mg/day. All solutions were kept on a hotplate

Restricted access

R. F. Parrott, S. N. Thornton, M. L. Forsling and C. E. Delaney

ABSTRACT

The effect of stress on drinking, water balance and endocrine profile was studied using ten castrated rams. Individual sheep were exposed to 30-h periods of total isolation (psychological stress) or physical separation from their social group (control). Plasma was analysed for haematocrit, osmolality, electrolyte levels and concentrations of cortisol and arginine vasopressin. Isolation stress significantly reduced water intake, increased haematocrit and plasma concentration of cortisol, but did not alter osmolality or vasopressin concentration. The physiological effects of this self-imposed water restriction contrast with those obtained by depriving the sheep of water for 24 h under conditions that were not stressful, i.e. by keeping them grouped together. These results suggest that cortisol may act to defend plasma volume in sheep exposed to acute stress. The results also indicate that vasopressin probably should not be considered to be a 'stress hormone' in the sheep.

J. Endocr. (1987) 112, 305–310

Restricted access

CYNTHIA DOUGHTY, JANET E. BOOTH, P. G. McDONALD and R. F. PARROTT

SUMMARY

Groups of neonatal female rats were treated for the first 5 days of life with oestradiol-17β, oestradiol benzoate or a synthetic oestrogen, 11β-methoxy-17-ethynyl-1,3,5(10)-oestratriene-3,17β-diol (RU 2858), in daily doses ranging from 0·5 to 1000 ng. Oestradiol-17β had no effect on adult ovarian cyclicity or sexual receptivity after ovariectomy and oestrogen + progesterone treatment. Ovarian cyclicity was prevented by 100 ng or more oestradiol benzoate/day, and by all doses of RU 2858. Only rats receiving 50 ng oestradiol benzoate/ day or 0·5 ng RU 2858/day showed normal receptivity. The defeminizing action of RU 2858 was at least 100 times greater than that of oestradiol benzoate; it is suggested that this greater potency is due to the low affinity of RU 2858 for the oestradiol-binding protein in the plasma of neonatal rats. These results indicate that defeminization of the neonatal rat brain can be induced by physiological amounts of oestrogen, and are discussed with reference to the action of testosterone.

Restricted access

CYNTHIA DOUGHTY, JANET E. BOOTH, P. G. McDONALD and R. F. PARROTT

Department of Physiology, The Royal Veterinary College, Royal College Street, London, NW1 OTU

(Received 24 March 1975)

Neonatal treatment of female rats with testosterone will prevent the cyclic pattern of gonadotrophin secretion and sexual receptivity in adulthood (Barraclough, 1961). This effect probably depends on the production of small amounts of oestrogen from testosterone in the brain (Reddy, Naftolin & Ryan, 1974) since non-aromatizable androgens do not have this effect (McDonald & Doughty, 1974). Antagonism of testosterone-induced masculinization by the anti-oestrogen MER-25 (ethamoxytriphetol; McDonald & Doughty, 1973/74; Doughty & McDonald, 1974) supports this hypothesis. Neonatal treatment with very low doses of the synthetic oestrogen RU 2858 (11β-methoxy-17-ethynyl-1,3,5,(10)-oestratriene-3,17β-diol) will also defeminize the female brain (Doughty, Booth, McDonald & Parrott, 1975). The object of this study was to prevent defeminization, induced by neonatal treatment with RU 2858, with the anti-oestrogen MER-25.

Starting within 24 h of birth (day 1) and continuing for 5