Ovarian steroid production in vitro during gonadal regression in the turkey. I. Changes associated with incubation behavior.

The mechanism regulating ovarian regression during incubation behavior in the domestic turkey has not been elucidated. This study was designed to determine whether ovarian steroidogenic potential is depressed during gonadal regression associated with the onset of incubation behavior. Hens were housed in floor pens equipped with trap nests that were checked 7 times per day. Hens were grouped, according to nesting frequency and egg production, into the following classifications: laying (laid an egg every day and trapped in the nest only once/day); transitional (laid an egg every day but trapped in the nest 4 or more times/day); and Day 1, Day 3, and Day 5 incubating (no egg for 2, 4, or 6 days, respectively, while trapped in the nest at least 4 times/day). Follicular atresia was evident in the largest preovulatory follicle (F1) in transitional hens, extensive in F1 through the third largest follicle (F3) in Day 1 incubating hens, and extensive in F1 through F7in Day 3 incubating hens. Levels of circulating LH, progesterone (P), androgen (A), and estradiol (E) decreased in transitional hens relative to concentrations in laying hens and remained low thereafter. In contrast, levels of prolactin were greater in Day 3 and Day 5 incubating hens than in laying, transitional, or Day 1 incubating hens. Basal production of P by F1 granulosa cells was lower from Day 1 incubating hens than from the other groups. Production of P in response to porcine-luteinizing hormone (pLH) was greater by cells from transitional and Day 1 incubating hens than from those of laying hens.(ABSTRACT TRUNCATED AT 250 WORDS)     

Elevated peripheral concentrations of LH block ovulation and increase thecal and serum progesterone in the hamster

Insertion of osmotic minipumps containing 1 mg ovine LH on Day 1 (oestrus) elevated circulating serum concentrations of LH, progesterone and androstenedione when compared with values at pro-oestrus. Ovulation was blocked for at least 2 days at which time there were twice the normal numbers of preovulatory follicles. Follicular and thecal progesterone production in vitro was elevated when compared with that in pro-oestrous controls. Follicular and thecal androstenedione production in vitro was lower than in controls even though serum concentrations of androstenedione were elevated; the higher androstenedione values may be due to the increase in number of preovulatory follicles when compared with pro-oestrous controls. Follicles from LH-treated hamsters aromatized androstenedione to oestradiol and follicular production of oestradiol was similar to that in pro-oestrous follicles despite low follicular androstenedione production in the LH-treated group. Treatment with 20 i.u. hCG on Days 4 or 6 after insertion of an LH osmotic minipump on Day 1 induced ovulation of approximately 30 ova, indicating that the blockade of ovulation was not due to atresia of the preovulatory follicles. Serum progesterone concentrations on Days 2, 4 and 6 in LH-treated hamsters were greater than 17 nmol/l, suggesting that the blockade of ovulation might have been due to prevention of the LH surge by high serum progesterone concentrations.     

Progesterone injection and egg production in turkey hens

An arrest in laying associated with either a polyovarian follicle (POF) or a polycystic ovarian follicle (PCOF) syndrome has been reported in turkey hens photostimulated at an early age with a constant-light photoperiod. Hens expressing the POF or PCOF syndrome had stopped laying for several weeks, but the ovary contained an increased number of mature-size and larger follicles (POF hens), which were cystic (PCOF) in some of the hens. Hens with the POF or PCOF syndrome had plasma progesterone (P(4)) concentrations that were relatively high and without surges. We hypothesized that high plasma P(4) concentrations may block ovulatory surges of LH but not the growth or maintenance of hierarchical follicles leading to development of the POF or PCOF syndrome in turkey hens. In the first six studies, hens were photostimulated with either a 14L:10D or a 24L:0D photoperiod and, after laying for 1-38 wk, were then injected daily for up to 14 days with P(4) (up to 1.50 mg kg(-1) day(-1)) and necropsied. At all ages, the oviposition rate was reduced at a P(4) dosage of 0.17 mg kg(-1) day(-1). With dosages of 0.33 mg kg(-1) day(-1) or greater, however, ovipositions stopped in most hens within approximately 2 days. For hens laying for less than 15 wk, oviductal weight and number of hierarchical follicles of P(4)-injected hens were not different from control vehicle-injected hens, but the numbers of mature, cystic, and atretic follicles were increased. For hens laying for 38 wk, when treated with P(4), oviductal weight and number of hierarchical follicles decreased, but number of atretic follicles increased. No effect of photoperiod was found on egg production, oviductal weight, or follicle number, and none of the hens developed POF or PCOF syndrome in these experiments. Two additional experiments were conducted with hens early in the reproductive period that had been photostimulated with 14L:10D or 24L:0D and injected with P(4) (0.33 mg kg(-1) day(-1)) for 10 or 12 days but not necropsied until 3 wk after the last injection. Most of the hens photostimulated with the 24L:0D photoperiod and injected with P(4), and a few of the hens photostimulated with the 14L:10D photoperiod and injected with P(4), had developed the PCOF syndrome when necropsied. The hens with the PCOF syndrome had high levels of P(4) when necropsied. From these studies, we concluded that the PCOF syndrome can be induced early in the reproduction period by photostimulating turkey hens with a 24L: 0D photoperiod, injecting them for 10 to 12 days with P(4) at a dosage of 0.33 mg kg(-1) day(-1), and then waiting 3 wk for the PCOF syndrome to develop.     

Effects of early prenatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on postnatal reproduction in the laying hen (Gallus gallus)

This study demonstrates the long-term effects of very early embryonic exposure to a single dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (0, 10 and 20 ng/egg), administered before the beginning of embryonic development, on growth and reproductive performance in laying hens. Hatchability and body weight gain from 11 weeks onwards were significantly depressed in 20 ng treated hens. All hens started laying egg at around the same age and the laying performance of TCDD-treated hens was normal. No disturbances in the age-related pattern and concentrations of oestradiol, LH or FSH in plasma could be found but mean progesterone concentrations were significantly lower in 20 ng treated hens. Moreover, follicular distribution was changed with less small white follicles and smaller yellow follicles, which probably resulted in the lower egg weight of the 20 ng treated hens. At 43 weeks of age, hens treated in ovo with TCDD showed a retained right oviduct, mostly filled with clear fluid. From these results, it seems that in ovo exposure to TCDD interferes in the right oviduct regression during embryonic development and induces some changes in follicular distribution but without impairment of reproductive performance in the adult laying hen.     

Relative roles of oestradiol and of the uterus in the maintenance of the corpus luteum in the pseudopregnant brown hare (Lepus europaeus)

Brown hares were made pseudopregnant by sterile matings or PMSG-hCG treatment (day of mating or hCG injection = Day 0 of pseudopregnancy). Progesterone secretion by the CL began 3-4 days after the ovulatory stimuli, reached maximum on Days 8 to 11 and decreased thereafter to reach low levels from Day 9 to 18, depending on the female. Cauterization of all large ovarian follicles on Day 7 resulted in an immediate luteolysis in young females, but had no effect in older ones. Oestradiol capsules implanted from Day 7 to Day 46 were able to maintain progesterone secretion until at least Day 30, in intact females as well as in females with all large follicles cauterized. Hysterectomy on Day 7 or 8 was followed by an immediate drop in progesterone concentrations; oestradiol capsules implanted at the time of hysterectomy prevented the drop in progesterone values, which remained elevated until Day 38. The induction of ovulation in females hysterectomized 2 months before resulted in CL of slightly shortened life-span. The injection of PGF-2 alpha on Day 7 of pseudopregnancy was followed by an immediate luteolysis. These results suggest that oestradiol secreted by the large ovarian follicles is the main luteotrophic factor in the brown hare. In old hares, the large amount of interstitial tissue could secrete oestrogens, and thus maintain pseudopregnancy. On Day 7 of pseudopregnancy, the uterus secretes a luteotrophic substance acting either directly on the ovary, or via the pituitary, to maintain oestradiol secretion by the follicles. In long-term hysterectomized females, the CL would be able to develop independently of any trophic substance, but for a reduced duration.     

Effects of prostaglandin and prolactin on luteolysis and parturient behaviour in the non-pregnant tammar, Macropus eugenii

In Exp. 1 non-pregnant female tammars were injected, on Day 26 (the day parturition would normally occur) after removal of pouch young, with saline, 200 micrograms ovine prolactin or 5 mg PG and changes in plasma concentrations of progesterone, prolactin, PGF-2 alpha metabolite (PGFM), oestradiol-17 beta and LH were determined. Luteolysis occurred in females treated with prolactin alone, while treatment with PG first induced a rapid rise in prolactin and subsequently a significant decrease in plasma progesterone. After prolactin treatment the oestradiol peak, oestrus and the LH surge were advanced significantly compared to the saline-treated females. In Exp. 2 the effects of the same treatments as used in Exp. 1 were determined on Day 23 and again on Day 26 after removal of pouch young in non-pregnant females. On Day 23 both prolactin and PG induced significant elevations in plasma progesterone, but luteolysis did not occur. On Day 26 the treatments initially induced significant elevations in plasma progesterone but these were followed by luteolysis within 8-12 h after treatment. PG treatment induced parturient behaviour in the non-pregnant females within 3-21 min and this persisted during the period that plasma concentrations of PGFM were elevated. The results show that PG induces birth behaviour and the release of prolactin, while prolactin first induces an elevation of plasma progesterone concentrations and, in the mature CL on Day 26, subsequently induces luteolysis.     

Comparison of mammalian luteinizing hormone releasing hormone (LH-RH), and of an analog (ICI 118630), on luteinizing hormone and ovarian steroid (progesterone, oestradiol) secretions in laying hens. (Gallus domesticus)

This experiment was conducted to compare the luteinizing hormone (LH), progesterone (P4) and oestradiol (E2) release in response to injections of various doses of synthetic mammalian luteinizing hormone-releasing hormone (LH-RH) and of an LH-RH agonist, ICI 118630, administered to laying hens 4 to 9 hours after a mid-sequence ovulation. Plasma LH increased significantly within 10 minutes of injection of either compound whereas any increases in plasma steroid concentrations were discerned later, at approximately minutes post-injection. No dose-response relationship was found for either compound with respect to LH release, but ICI 118630 appeared more potent than LH-RH. This analog also produced a greater mean incremental rise in plasma progesterone, but not oestradiol, than LH-RH, and this was found in animals injected at a time when the largest ovarian follicle was not mature. These result suggest that ICI 118630 is a more potent releasing hormone in the hen at the level of the pituitary, and that it may have a stimulating effect on ovarian progesterone secretion.     

Ovarian steroid production in vitro during gonadal regression in the turkey. II. Changes induced by forced molting.

In the turkey, the onset of incubation behavior is associated with altered ovarian steroidogenesis, ovarian regression, decreased, LH secretion, and increased serum prolactin (Prl) levels. To clarify the relative contribution of circulating LH and Prl to the initiation of ovarian regression, laying hens were exposed for 0, 3, 7, or 14 days to a forced molting procedure (exposure to reduced day length of 6L:18D and removal of feed and water for the initial 3 days) that induces ovarian regression and decreased LH levels but does not increase Prl levels. On each of these days, hens were killed and granulosa and theca interna cells from the largest (F1) and fifth largest (F5) preovulatory follicles and total cells from the small white follicles (SWF) were incubated for 5 h in the presence or absence of ovine LH (oLH; 0-1,000 ng/ml). Force-molted hens exhibited diminished levels of circulating LH, Prl, progesterone (P), androgen (A), and estradiol (E) by Day 3 of treatment. Ovarian atresia began in F1 by the third day of treatment, and included F1 and F5 by the seventh day. No preovulatory follicles were present on the fourteenth day. With both F1 and F5 granulosa cells, production of P in the presence of oLH was initially enhanced (Day 3) and later absent (Day 7). In contrast, production of A by F5 theca interna cells in the presence of oLH was initially suppressed (Day 3) and then returned to pretreatment levels (Day 7).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of LH on progesterone and oestradiol production in vivo and in vitro by preovulatory rat follicles

Temporal changes in follicular oestradiol production induced in vitro and in vivo by LH were studied. In-vitro changes were measured by incubating preovulatory rat follicles for 12 h, changing the medium every 2 h. Follicles isolated at various intervals after an injection of 10 i.u. hCG were incubated for 2 h to measure changes in oestradiol production in vivo. In both studies there was an increase in oestradiol production lasting 4 h followed by a sharp decline. Progesterone production was also increased by LH in vitro or hCG in vivo, but remained high. A second exposure to LH did not raise oestradiol synthesis, but increased progesterone synthesis in vitro only. The decline in oestradiol production is most probably due to a decrease in C17-20 lyase activity, because addition of testosterone, but not of 17 alpha-hydroxyprogesterone, increased oestradiol production. Incubation of preovulatory follicles in the absence of LH or incubation of follicles derived from animals in which the spontaneous LH surge was blocked by an injection of pentobarbitone sodium also resulted in a decrease of oestradiol and an increase in progesterone production. This oestrogen-progesterone shift was also caused by a decrease in C17-20 lyase activity. The results demonstrate that the changes in steroid production in vivo and in vitro are similar and occur in the presence and absence of LH. It is concluded that the decrease in oestradiol production is dependent on the decrease in the activity of enzymes converting progesterone to aromatizable androgens.     

Ability of progesterone to reverse anti-androgen (hydroxyflutamide)-induced interference with the preovulatory LH surge and ovulation in PMSG-primed immature rats

In Exp. 1, PMSG was injected to 26-day-old prepubertal rats to induce ovulations. On Day 2 (2 days later, the equivalent of the day of pro-oestrus) they received at 08:00 h 5 mg hydroxyflutamide or vehicle and at 12:00 h 2 mg progesterone or testosterone or vehicle. Animals were killed at 18:00 h on Day 2 or at 09:00 h on Day 3. Progesterone but not testosterone restored the preovulatory LH surge and ovulation in hydroxyflutamide-treated rats. In Exp. 2, 2 mg progesterone or testosterone were injected between 10:30 and 11:00 h on Day 2, to advance the pro-oestrous LH surge and ovulation in PMSG-primed prepubertal rats. Injection of hydroxyflutamide abolished the ability of progesterone to advance the LH surge or ovulation. Testosterone did not induce the advancement of LH surge or ovulation. In Exp. 3, ovariectomized prepubertal rats implanted with oestradiol-17 beta showed significantly (P less than 0.01) elevated serum LH concentrations at 18:00 h over those observed at 10:00 h. Progesterone injection to these animals further elevated the serum LH concentrations at 18:00 h, in a dose-dependent manner, with maximal values resulting from 1 mg progesterone. Hydroxyflutamide treatment significantly (P less than 0.003) reduced the serum LH values in rats receiving 0-1 mg progesterone but 2 mg progesterone were able to overcome this inhibition. It is concluded that progesterone but not testosterone can reverse the effects of hydroxyflutamide on the preovulatory LH surge and ovulation. It appears that hydroxyflutamide may interfere with progesterone action in induction of the LH surge, suggesting a hitherto undescribed anti-progestagenic action of hydroxyflutamide.     

Gonadotrophic control of steroidogenesis in human granulosa-lutein cells

Granulosa-lutein cells were harvested from periovulatory follicles in human ovaries and cultured for up to 6 days, equivalent to almost half of a normal luteal phase. The average rate of basal progesterone accumulation in the culture medium was constant at approximately 36 nmol progesterone/10(6) cells/day. Oestradiol accumulation was too low to measure in the absence of precursor androgen. Basal aromatase activity (measured as oestradiol formed in 3 h from 10(-6) M exogenous testosterone) was high (average 1.15 nmol oestradiol/10(6) cells/3 h) at the time of cell isolation (Day 0) but fell by greater than 90% on Day 1. By Day 2 the activity had partly recovered and averaged 62% of the Day 0 value, rising to 70% on Day 6. This loss and recovery of aromatase activity was independent of the addition of gonadotrophic hormones to the culture medium. However, dose-related increases in aromatase activity occurred in the presence of highly pure human pituitary LH (0.1-30 ng/ml). The increase was observed on Day 4 and was maximal on Day 6 (average 3-fold increase over control) in the presence of LH concentrations greater than or equal to 1.0 ng/ml. LH also caused dose-related increases in progesterone accumulation by Day 4 with maximal stimulation on Day 6 (average 3-fold increase over control) at greater than or equal to 10.0 ng/ml. Dose-related stimulation of aromatase activity by human pituitary FSH also occurred but maximal stimulation required the presence of 300 ng FSH/ml and progesterone accumulation was hardly affected at this dose.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationship between concentrations of cortisol in ovarian follicular fluid and various biochemical markers of follicular differentiation in cyclic and anovulatory cattle

Concentrations of cortisol were determined in pooled fluid of small (less than 10 mm) and large (greater than or equal to 10 mm) follicles of cyclic cattle (Exp. 1), and in fluid of the largest follicle of 17 post-partum anovulatory cows (Exp. 2). In Exp. 1, concentrations of cortisol in small follicles were greater (P less than 0.05) than in large follicles (14.7 versus 13.2 ng/ml), and varied significantly with stages of the cycle; small and large follicles had the highest cortisol concentration during the early luteal phase of the cycle. Large follicles had 2-fold greater concentrations of oestradiol than did small follicles, whereas small follicles had 2-fold greater concentrations of androstenedione than did large follicles. Across pools of follicular fluid, cortisol concentrations were correlated only to androstenedione concentrations (r = 0.65, P = 0.07). In Exp. 2, concentrations of cortisol did not significantly differ between oestrogen-active (oestradiol greater than progesterone in follicular fluid) and oestrogen-inactive (progesterone greater than oestradiol) follicles, although oestrogen-active follicles had a 24-fold greater concentration of oestradiol than did oestrogen-inactive follicles. Cortisol concentrations were correlated to hCG binding capacity of thecal cells (r = -0.35, P = 0.08) and to follicular diameter (r = 0.45, P less than 0.05). These results suggest that normally fluctuating concentrations of cortisol in follicular fluid of cattle play little or no active role in follicular differentiation in vivo.     

Age-dependent changes in the hypothalamo-pituitary-ovarian axis of the laying hen.

The functional integrity of the components of the hypothalamo-pituitary-ovarian axis was examined in young and old laying hens. Ovarian function was tested by measuring the amount of progesterone released in response to an injection of LH, and pituitary function was investigated by measuring the increase in the plasma LH level after an injection of LH-RH. There were no differences between young and old birds in the response of the pituitary gland or the ovary to these stimuli. Hypothalamic function was investigated by studying the positive feedback action of a standard dose of progesterone on LH release; the positive feedback response was smaller (P less than 0.05) in old hens. It is suggested that the fall in the rate of lay in hens towards the end of their laying year is caused partly by a decrease in the response of the LH-positive feedback mechanism to progesterone.     

Progesterone pretreatment has a direct effect on GnRH-induced preovulatory follicles to determine their ability to develop into normal corpora lutea in anoestrous ewes

In two experiments carried out during seasonal anoestrus, Romney Marsh ewes were treated with small-dose (250 ng) multiple injections of GnRH at 2-h intervals with and without progesterone pretreatment. In Exp. 1, 8/8 progesterone-primed ewes ovulated and produced functionally normal corpora lutea compared with 2/9 non-primed ewes. Follicles were recovered from similarly treated animals 18 or 28 h after the start of GnRH treatment (at least 14 h before the estimated time of the LH peak) and assessed in terms of diameter, granulosa cell number, oestradiol, testosterone and progesterone concentrations in the follicular fluid, oestradiol production in vitro and binding of 125I-labelled hCG to granulosa and theca. There were no significant differences in any of these measures in 'ovulatory' follicles recovered from the progesterone-pretreated compared to non-pretreated animals. In Exp. 2, follicles were removed from similar treatment groups just before and 2 h after the start of the LH surge. Unlike 'ovulatory' follicles recovered from the non-pretreated ewes, those recovered from progesterone-pretreated ewes responded to the LH surge by significantly increasing oestradiol secretion (P less than 0.01) and binding of 125I-labelled hCG (P less than 0.05) to granulosa cells. Overall there was also more (P less than 0.05) hCG binding to granulosa and theca cells from progesterone-pretreated animals. Non-ovulatory follicles recovered from progesterone-primed ewes had more (P less than 0.05) binding of 125I-labelled hCG to theca and a higher testosterone concentration in follicular fluid (P less than 0.05) than did those from non-primed ewes. These results suggest that inadequate luteal function after repeated injections of GnRH may be due to a poor response to the LH surge indicative of a deficiency in the final maturational stages of the follicle.     

Episodic secretion of gonadotrophins and ovarian steroids in jugular and utero-ovarian vein plasma during the follicular phase of the oestrous cycle in gilts

Blood samples were collected simultaneously from the jugular and utero-ovarian veins of 13 gilts from Days 11 through 16 of the oestrous cycle. A luteolytic dose (10 mg) of PGF-2 alpha was given on Day 12 to facilitate the natural occurrence of luteolysis and standardize the associated decrease in concentrations of progesterone. The mean interval from PGF to oestrus was 5.5 +/- 0.7 days (mean oestrous cycle length = 17.5 +/- 0.7 days). Mean concentrations, pulse amplitudes and pulse frequencies of oestradiol and progesterone were greater (P less than 0.05) in the utero-ovarian than jugular vein. Secretory profiles of LH and FSH were similar (P greater than 0.05) in plasma collected simultaneously from both veins. Based on these data, temporal relationships among hormonal patterns of FSH and LH in the jugular vein and oestradiol and progesterone in the utero-ovarian vein were examined. Concentrations of progesterone declined (P less than 0.05) between Days 12 and 14, while all secretory variables for oestradiol increased (P less than 0.05) from Day 12 through 16 of the oestrous cycle. The pulsatile secretion of FSH remained relatively constant during the experiment. However, both pulse amplitude and mean concentration tended (P less than 0.2) to be lower on Day 16 compared with Day 12. The episodic secretion of LH shifted from a pattern characterized by high-amplitude, low-frequency pulses to one dominated by numerous pulses of diminishing magnitude between Days 13 and 14. From Days 14 to 16 of the oestrous cycle, 91% of all oestradiol pulses were temporally associated with gonadotrophin pulses composed of both FSH and LH episodes. However, pulses of oestradiol (52%) not associated with an episode of LH and/or FSH were observed on Days 12 and 13. These data demonstrate that during the follicular phase of the pig oestrous cycle substantial oestradiol production occurred coincident with luteolysis and before the shift in the episodic secretion of LH. The pool of follicles which ovulated was probably the source of this early increase in the secretion of oestradiol. Therefore, we propose that factors in addition to FSH and LH are involved in the initial selection of follicles destined to ovulate during the early stages of the follicular phase of the pig oestrous cycle. In contrast, high-frequency, low-amplitude pulses composed of LH and FSH were the predominant endocrine signal associated with oestradiol secretion during the second half of the oestrous cycle.(ABSTRACT TRUNCATED AT 400 WORDS)     

Neuroendocrine control of reduced persistence of egg-laying in domestic hens: evidence for the development of photorefractoriness.

Egg-laying in hens exposed for more than 11 months to photostimulatory daylengths was intermittent and associated with a reduction in numbers of yellow-yolky ovarian follicles. Old laying hens (105 weeks) had lower concentrations of luteinizing hormone (LH) in the pituitary gland and plasma and reduced pituitary gland responsiveness to chicken LH-releasing-hormones (LHRH-I and II) in vivo when compared with young laying hens (28 weeks). Four weeks after transfer from 14 to 8 h light/day, egg production almost stopped in old, but not in young hens, although plasma LH concentrations decreased in all birds. After transfer from 14 to 20 h light/day, plasma LH increased in young, but not in old, hens, without a change in the rate of egg production. Reproductive function was enhanced in old hens returned to long days after induction of a moult and ovarian regression by reducing daylength and dietary restriction. Moulted hens had a greater rate of egg production, higher concentrations of plasma LH and a greater pituitary-gland responsiveness to LHRH-II in vivo than unmoulted control hens. After transfer from 14 to 8 h light/day, egg-laying decreased more rapidly in unmoulted than in moulted hens; transfer to 17 h light/day increased egg production in moulted, but not in unmoulted, birds. Induction of ovarian regression in old hens by dietary restriction alone also enhanced reproductive function after the dietary restriction was relaxed. Egg-laying was more persistent in hens brought into lay for a second year by transferring them from 3 to 11 h light/day than in hens transferred from 3 to 20 h light/day. Egg production was stimulated in hens maintained on 3 or 11 h light/day for 42 weeks, after transfer to 20 h light/day. Egg production ceased in hens maintained on 20 h light/day for 46 weeks, after transfer to 3 h light/day. These observations are consistent with the view that poor persistence of laying in hens less than 2 years old and exposed continuously to long days is caused, in part, by a reduction in hypothalamic-gonadotroph function. This reduction in neuroendocrine function may be due, in part, to the development of relative photorefractoriness.     

Oestradiol-17beta, progesterone, FSH and LH in prepubertal calves induced to superovulate

Fluorogestone acetate (vaginal sponge for 4 days) and PMSG (i.m. injection at the time of sponge insertion) treatment was administered to seven 3-month-old calves to induce superovulation. Samples of peripheral plasma were taken every 4 h during treatment (4 days) and then every 2 h for 7 days. FSH, LH, oestradiol and progesterone were measured by radioimmunoassays. In all calves oestradiol concentrations increased 24 h after PMSG injection and reached the highest levels (41-502 pg/ml) during the preovulatory surge of both gonadotropins. The surge of LH and FSH occurred from 12 to 22 h after cessation of treatment. The maximum levels of LH and FSH were 11-72 ng/ml and 23-40 ng/ml respectively and occurred within 4 h of each other. Between 40 and 68 h after the LH peak the concentrations of progesterone began to increase from basal values, reaching 24.0-101.7 ng/ml when the animals were killed. A quantitative relationship was found between plasma oestradiol concentration and the numbers of ovulating follicles. Progesterone levels seemed to be related to the numbers of corpora lutea and also to the numbers of unovulated follicles. Gonadotrophin output was not quantitatively related to ovarian activity or to steroid secretion.     

A Combination of Zinc and Pyridoxine Supplementation to the Diet of Laying Hens Improves Performance and Egg Quality

The objective of this study was to investigate whether zinc, along with pyridoxine, is effective in improving performance and egg quality of laying hens. One hundred and twenty, 28-week-old Hy-Line laying hens were assigned to four treatment groups, 30 hens each. The birds were fed a basal diet or the basal diet supplemented with either 30 mg of zinc/kg of diet, 8 mg of pyridoxine/kg of diet, or 30 mg of zinc plus 8 mg of pyridoxine/kg of diet. Feed conversion (P < 0.01) and egg production (P < 0.01) improved most when both zinc and pyridoxine were supplemented to the diet. Eggshell weights were also greatest (P < 0.01) when the diet was supplemented with both pyridoxine and zinc. Egg-shape index was, however, greatest with zinc-supplemented diet (P < 0.004). Haugh unit was greatest in eggs of hens fed a diet supplemented with both zinc and pyridoxine (P < 0.01). Dietary zinc and pyridoxine supplementations together increased plasma calcium and phosphorous concentrations (P < 0.002). The results of the present study suggested that zinc (30 ppm) and pyridoxine (8 ppm) supplements, when used together, are recommended in terms of a better performance and egg quality in laying hens.     

Contrasting effects of oestradiol-17 beta and human chorionic gonadotrophin on steroidogenesis in the rabbit corpus luteum

On Day 10 of pseudopregnancy, rabbits were given an i.v. injection of hCG (10-20 i.u.) that was sufficient to cause new ovulations and the loss of follicular oestradiol secretion. There was an immediate 3-4-fold rise in serum progesterone which returned to near prestimulation values (approximately 27 ng/ml) within 12 h in the presence of an implant containing oestradiol-17 beta. In the absence of oestradiol, serum progesterone continued to decline to reach low values (approximately 4 ng/ml) within 24 h and the original corpora lutea subsequently regressed. The administration of oestradiol 24 h after injection of hCG, when progesterone secretion was low, arrested any further decline in progesterone and then restored serum progesterone to normal values. This steroidogenic effect of oestradiol in vivo was a function of enhanced luteal steroidogenesis; corpora lutea removed and incubated for 12 h produced progesterone at high, linear rates, whereas the corpora lutea from animals that did not receive oestradiol produced low or insignificant quantities of progesterone in vitro. We conclude that hCG at these doses is compatible with continued responsiveness of the corpora lutea to oestrogen and that hCG produces its luteolytic effect primarily by ovulating follicles, thus stopping the secretion of the luteotrophic hormone, oestradiol.