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A. S. McNeilly, D. H. Abbott, S. F. Lunn, P. C. Chambers and J. P. Hearn

Summary. A heterologous double-antibody radioimmunoassay was used to measure plasma prolactin concentrations in 27 marmosets. The assay was valid for the marmoset because plasma levels of prolactin were increased in response to TRH and metoclopramide and suppressed in response to bromocriptine treatment.

During the cycle there were no consistent changes in plasma prolactin concentrations. During lactation mothers suckling single or twin infants had higher prolactin levels than did non-suckling females and levels were highest with twins. No statistically significant delay in the resumption of ovulation post partum was observed for the suckling and non-suckling females; conception occurred in all but one marmoset by 70 days post partum.

These results show that neither the suckling stimulus nor high levels of prolactin post partum delay the return of ovulation and fertility in the common marmoset, a result in contrast to that for all other primate species so far investigated.

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D. H. Abbott, A. S. McNeilly, S. F. Lunn, M. J. Hulme and F. J. Burden

Summary. Plasma concentrations of progesterone, cortisol, LH and prolactin were measured in dominant and subordinate female marmosets in 10 well-established peer groups. Subordinate females never ovulated, had a reduced LH response to LH-RH and showed no positive feedback LH surge after oestrogen administration. There was no evidence of elevated plasma cortisol levels or hyperprolactinaemia in subordinates and all showed a similar prolactin response to TRH in comparison with dominants. However, subordinates showed a reduced prolactin response to metoclopramide. These results clearly indicate that high circulating levels of cortisol or prolactin are not responsible for the inhibition of ovulation in female marmosets.

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M. Mondain-Monval, O. M. MØller, A. J. Smith, A. S. McNeilly and R. Scholler

Summary. A heterologous radioimmunoassay system developed for the rabbit and suitable for a wide range of mammalian species has been shown to measure prolactin in the plasma of the blue fox. Evaluation of prolactin levels throughout the year showed that concentrations displayed a circannual rhythm with the highest values occurring in May and June. Prolactin concentrations remained low (∼2·5 ng/ml plasma) from July until April with no consistent changes found around oestrus (March—April). In 8 pregnant females, the prolactin increase in late April and May coincided with the last part of gestation and lactation: concentrations (mean ± s.e.m.) increased to 6·3 ± 0·6 ng/ml at mid-gestation, 9·7 ± 2·1 ng/ml at the end of gestation and 26·7 ± 5·0 ng/ml during lactation. In 10 non-pregnant animals, the mean ± s.e.m. values were 7·2 ± 1·2 ng/ml in April, 8·8 ± 2·2 ng/ml in May and 9·8 ± 1·3 ng/ml in June. The prolactin profile in 4 ovariectomized females was similar to that observed in non-pregnant animals, but the plasma values tended to be lower during the reproductive season (April—June). In intact females, the only large LH peak (average 28 ng/ml) was observed around oestrus. During pro-oestrus, baseline LH levels were interrupted by elevations of 3·1–10·4 ng/ml. During the rest of the year, basal levels were < 3 ng/ml. In ovariectomized females, LH concentrations increased within 2 days of ovariectomy and remained high (35–55 ng/ml) at all times of year.

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M. Mondain-Monval, A. J. Smith, P. Simon, O. M. Møller, R. Scholler and A. S. McNeilly

Summary. A heterologous radioimmunoassay system developed for the sheep was shown to measure FSH in the plasma of the blue fox. FSH concentrations throughout the year showed a circannual rhythm with the highest values (61 ·6 ± 14·8 ng/ml) occurring shortly before or at the onset of the mating season, a pattern similar to that of LH. The concentration of FSH then declined when androgen concentrations and testicular development were maximal at the time of the mating season (March to May). Thereafter, concentrations remained low (25·2 ± 4·1 ng/ml) in contrast to those of LH. Implantation of melatonin in August and in February maintained high plasma values of FSH after the mating season (142·3 ± 16·5 ng/ml) in association with a maintenance of testicular development and of the winter coat. The spring rise of prolactin was suppressed by melatonin treatment. The release of FSH after LHRH injection was also increased during this post-mating period in melatonin-treated animals, in contrast to the response of the control animals which remained low or undetectable.

These results suggest that changes both in the secretions of FSH and prolactin may be involved in the prolongation of testicular activity and in the suppression of the spring moult after melatonin administration.

Keywords: blue fox; FSH; melatonin; LHRH; seasonal cycle

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H. M. Fraser, A. S. McNeilly, M. Abbott and R. A. Steiner

Summary. A dose of 100 μl of a potent ovine LHRH gamma globulin inhibited ovulation in the cyclic rat when administered at 12:00 h on the day of pro-oestrus. A dose of 10 ml of the preparation was administered i.v. to female stumptailed macaques to achieve circulating antibody titres 3–4-fold higher than in the rat. In an ovariectomized macaque, this caused a marked fall in serum concentrations of LH to less than 10% of pretreatment values and also a significant, though less pronounced, fall in FSH. Six monkeys were treated with the LHRH gamma globulin during the mid—late follicular phase of the cycle. In 2 monkeys in which serum oestradiol concentrations were <100 pg/ml at the time of antibody administration, the rising oestradiol levels were abruptly suppressed and the normal mid-cycle LH surge failed to occur. Serum concentrations of LH and FSH declined to low levels for 8–10 days after which time normal follicular development occurred. In the remaining 4 monkeys in which follicular development was more advanced as indicated by serum oestradiol concentrations of >100 pg/ml, the antibodies induced either a transient decline or had no effect on the rising serum concentration of oestradiol. An LH/FSH surge followed by a rise in serum progesterone occurred in these macaques. When the antibodies were administered to a further 6 macaques, which had also been treated with oestradiol benzoate during the early follicular phase to induce an LH surge, the neutralization of LHRH again failed to block the surge even when the dose of antibody was increased to 20 ml.

The results show that LHRH antibodies were unable to block the LH surge in the macaque. They contrast with results obtained with LHRH immunoneutralization in the sheep, rat, hamster, mouse and bird and suggest that the ability of oestrogen to induce an LH surge by acting directly on the LHRH-primed anterior pituitary gland is more dominant in the primate.

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O Gubbay, W Guo, M T Rae, D Niven, A F Howie, A S McNeilly, L Xu and S G Hillier

The majority of ovarian cancers (>90%) are believed to derive from the ovarian surface epithelium (OSE); a single layer covering the entire surface of the ovary. At ovulation, the OSE cell layer undergoes an inflammatory response, involving cell death and growth, in order to overcome ovarian surface rupture. Abnormalities during these processes are believed to contribute to the development of tumours. Using primary cultures of OSE cells, we have compared anti-inflammatory and proliferative responses directly between human and ovine OSE cells to further establish the use of ovine OSE cells as a suitable model system for the study of human OSE cells. In order to compare effects of inflammatory stimulation, expression and activity of 11βhydroxysteroid dehydrogenase (11βHSD) type 1 was measured in OSE cells in response to interleukin (IL)-1α. As previously identified in human OSE cells, treatment of ovine OSE cells with IL-1α stimulated a concomitant increase of 11βHSD type 1 mRNA (31-fold; P < 0.05) and oxoreductase activity, indicating an increased production of anti-inflammatory cortisol. To compare the growth of human and ovine OSE cells, OSE cell number was measured in response to treatment with gonadotropins or growth factors. In the presence of FSH, LH or human chorionic gonadotropin (hCG), ovine and human OSE cell growth was similarly stimulated >1.2-fold (P < 0.05). In the presence of connective tissue growth factor (CTGF) and more significantly insulin growth factor I (IGF-I), human and ovine OSE cell growth was also similarly stimulated >1.2-fold (P < 0.05) and >1.5-fold (P < 0.01), respectively. The induction of both human and ovine OSE cell growth by IGF-I or hCG was further shown to be dependent on activation of the MAP kinase/extracellular-signal-regulated kinase (ERK) pathway. Stimulation of ovine OSE cell growth by hepatocyte growth factor (HGF) was similarly shown to be ERK-dependent; however, for human OSE cells, HGF only mildly stimulated ERK phosphorylation and failed to stimulate OSE cell growth. The demonstration that human and ovine OSE cells share similarities at the level of cell signalling, gene expression and cellular growth supports the use of ovine OSE cells as a suitable model for the study of human OSE cells.

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J. J. Robinson, R. P. Aitken, T. Atkinson, J. M. Wallace and A. S. McNeilly

Twelve anoestrous ewes maintained under natural photoperiod at 57°N received an oral dose of 3 mg melatonin daily at 15:00 h from 1 May. Starting 41 days later and extending from 11 June until 5 September, six of the ewes were also infused continuously with 0.8 mg thyrotrophin-releasing hormone (TRH) day−1 via subcutaneous osmotic minipumps. The remaining six ewes acted as controls. Behavioural oestrus, ovulation rate and luteal function were determined by exposure to a vasectomized ram, laparoscopy and the measurement of progesterone in peripheral plasma, respectively. TRH infusion stimulated a sustained increase (P < 0.001) in plasma concentrations of thyroxine, tri-iodothyronine and prolactin (thyroxine: 158 ± 9.3 and 65 ± 7.7 nmol l−1 for TRH-infused and control ewes, respectively; tri-iodothyronine, 2.6 ± 0.12 and 1.1± 0.19 nmol−1 and prolactin, 57±12 and 11 ± 2 μg l−1). No ewes were in oestrus before the TRH infusion and the mean number of behavioural oestrous cycles per ewe during the infusion period was 1.3 ± 0.33 and 2.5 ± 0.34 for TRH-infused and control ewes, respectively (P < 0.05). Corresponding mean intervals from 1 May to the onset of the first luteal phase (progesterone > 1 ng ml−1) were 88 ± 8.9 and 79 ± 3.5 days (not significant). TRH infusion had no effect on the mean numbers of corpora lutea (1.7 ± 0.14 and 1.6 ± 0.20 for TRH-infused and control ewes, respectively), but was associated with a lower mean incidence of normal luteal phases (1.5 ± 0.43 versus 2.7 ± 0.21, P= 0.052). Abnormalities in luteal function included delayed initial expression, extended ovarian cycles, suprabasal periovulatory progesterone concentrations and protracted periods of low progesterone secretion between successive ovarian cycles. Thus continuous TRH infusion suppressed plasma prolactin, doubled the circulating concentrations of thyroxine and tri-iodothyronine, and was associated with a wide range of abnormalities in ovarian function and endocrine status, the nature of which varied between ewes.

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B. K. Campbell, H. M. Picton, A. S. McNeilly and D. T. Baird

Summary. In Exp. 1, 7 Finn–Merino ewes which had one ovary autotransplanted to a site in the neck had jugular and timed ovarian venous blood samples collected at 10-min intervals for 2 h before and 3 h after injection of 5 μg NIAMDD-oFSH-S16. In Exp. 2, 8 Finn–Merino ewes with ovarian autotransplants had jugular and timed ovarian venous blood samples collected at 15-min intervals for 2 h before and 12 h after bolus injection of 40 μg NIAMDD-oFSH-S16 and infusion of oFSH-S16 at 6 μ/min for 4 h. In Exp. 2 the follicular population of the ovary was assessed by real-time ultrasound at the beginning and end of the experimental period.

In both experiments the secretion rates of inhibin (1–3 ng/min) and oestradiol (0·5–8 ng/min) were similar to those observed during the luteal phase of the cycle in the breeding season, indicating significant follicular development in these animals. In Exp. 1 there was no change in the secretion of oestradiol or inhibin after the injection of FSH which resulted in a 25% increase (P < 0·05) in the concentration of FSH in plasma. Inhibin secretion was pulsatile but there was no difference in inhibin pulse frequency before (1·6 ± 0·2 pulses/h) or after (1·2 ± 0·5 pulses/h) injection of FSH. In Exp. 2 injection of FSH resulted in an increase (P < 0·001) in plasma concentrations of FSH in the sample taken 10 min after injection from a baseline of 1·2 ± 0·2 ng/ml to a peak of 10·6 ± 1·0 ng/ml (mean ± s.e.m.). FSH concentrations remained elevated over pretreatment values for 10 h after the beginning of the treatment. The concentration of LH in jugular venous plasma increased (P < 0·001) after the bolus injection of FSH from a baseline of 1·4 ± 0·5 ng/ml to a peak of 6·7 ± 0·6 ng/ml. The ovarian rate of inhibin secretion did not change significantly following the injection and infusion of FSH. There was no difference in inhibin pulse frequency before (0·4 ± 0·2 pulses/h) or after 0·5 ± 0·1 pulses/h) injection of FSH. The rate of oestradiol secretion by the ovary increased (P < 0·001) after the injection of the FSH preparation, an effect that can be attributed to contamination of the FSH preparation with LH. Increasing jugular venous concentrations of FSH for 10 h had no effect on the ovarian follicle population.

We conclude that the ovarian secretion of inhibin is not acutely responsive to stimulation by FSH in anoestrous ewes.

Keywords: sheep; inhibin; FSH; ovary; anoestrus

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A. S. McNeilly, Morag Hunter, R. B. Land and H. M. Fraser

Summary. Scottish Blackface ewes were given LH-RH (3 × 30 μg i.v., at 90 min intervals) or D-Ser-(But)6-des Gly10 LH-RH ethylamide (LH-RH agonist) as a single injection (8 or 40 μg) during anoestrus. Ovulation as judged by laparoscopy occurred in 8 of the 27 animals. Despite the fact that the LH-RH agonist induced a greater release of LH and FSH the different treatments had no effect on the number of ewes ovulating and within each treatment group there was no apparent difference in the amounts of gonadotrophins released between the ewes that did or did not ovulate. All ovulations resulted in the formation of CL associated with plasma progesterone concentrations of <1 ng/ml (1–5 ng/ml in the normal luteal phase). In comparison with CL of the normal cycle the induced CL were of lower weight and had reduced progesterone content and ability to secrete progesterone in vitro. However, the binding of hCG was equivalent to that of normal CL.

These results suggest that the inadequate CL formed in anoestrous ewes after a single LH-RH injection have not developed the ability to synthesize and secrete progesterone in spite of the presence of normal amounts of LH receptors.

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J. J. Robinson, J. M. Wallace, R. P. Aitken and A. S. McNeilly

Thirty-two Scottish Blackface ewes that lambed outdoors in March and were weaned at the end of April and individually penned indoors under the natural photoperiod at 57°N were used to determine whether the ovine ovary that was deprived of gonadotrophic support was capable of early activation by melatonin. From 5 May (day 0), 16 of the ewes received an oral dose of 3 mg melatonin in a 4:1 (v:v) mixture of water and ethanol daily at 15:00 h. The remaining 16 ewes received the vehicle alone. Within each of these groups, eight were implanted s.c. on day 0 with an osmotic minipump which infused 50 μg of the gonadotrophin releasing hormone agonist (GnRHa), buserelin day−1. On day 25, a second minipump was inserted to ensure continued infusion of the agonist and on day 50 (24 June) both minipumps were removed. Ovarian activity was assessed by laparoscopy at intervals of 3 weeks from day 29 until the experiment was terminated on day 200 (21 November). Blood samples taken by jugular venepuncture three times a week for the first 50 days, daily from days 51–78 and thereafter three times a week were analysed for progesterone, prolactin and LH. Samples taken at intervals of 15 min for 10 h on days −1, 14, 28, 49, 56, 70 and 91 were assayed for LH. Treatment with GnRHa reduced LH concentrations and abolished pulsatile LH secretion. The onset of ovarian activity (progesterone >3.8 nmol l−1) was not affected by the 50-day GnRHa treatment and occurred for the melatonin-treated ewes at mean (± sem) intervals from 5 May of 66 ± 2.9 (range 51–75) and 71 ± 0.9 (range 68–75) days for non-GnRHa and GnRHa ewes, respectively. For the ewes not receiving melatonin the corresponding intervals were 113 ± 11.6 and 125 ± 9.2 days, respectively. The mean numbers of corpora lutea at first oestrus were not affected by GnRHa treatment and were 1.4 ± 0.13 and 1.5 ± 0.13 for control and melatonin-treated ewes, respectively. First ovulation following GnRHa treatment resulted in luteal concentrations of progesterone of normal duration and magnitude but, within the melatonin-treated ewes, those that received GnRHa returned to anoestrus 21 days earlier (P < 0.03) than did their non-GnRHa counterparts. After their initial suppression by melatonin, prolactin concentrations began to increase after 80 days of melatonin treatment in both non-GnRHa and GnRHa ewes and approximately three months before the ewes returned to anoestrus. The results demonstrate that a period of isolation of the ovaries of the ewe from the pituitary gonadotrophins does not alter their ability to respond to the melatonin-induced activation of the GnRH pulse generator.