Effects of luteinizing hormone, progesterone, testosterone, estradiol and corticosterone on ovulation and luteinizing hormone release in hens treated with aminoglutethimide

Aminoglutethimide (AG), an inhibitor of steroidogenesis, was administered s.c. to 5 groups of laying hens at a dose of 200 mg AG/kg body weight 9 h before expected midsequence ovulation. This dose has previously been demonstrated to consistently block ovulation. The injection of AG was followed by s.c. injections of: Group 1, 1.0 mg progesterone; Group 2, 0.1 mg estradiol-17 beta; Group 3, 1.5 mg corticosterone, all at 6 h prior to expected ovulation; Group 4, 1.0 mg testosterone at both 8 h and 5 h before expected ovulation; and Group 5, 25 micrograms of ovine luteinizing hormone (LH) at 8 and 50 micrograms ovine LH at 6 h before expected ovulation. For each group, 4 control hens were injected with AG and the appropriate vehicle. Blood samples were taken at 1- or 2-h intervals from the time of AG injection to the expected time of ovulation. The hens were killed 4 h after expected ovulation and examined for the occurrence of ovulation. In all hens injected with vehicle, ovulation and the preovulatory surges of progesterone, testosterone, estradiol-17 beta and LH were inhibited. The plasma concentration of corticosterone was not reduced following an injection of AG. Four of 6 hens ovulated in response to injection of ovine LH, although neither endogenous LH nor progesterone were released. Thus, LH appears to play a direct role in follicular rupture and extrusion of the ovum. The administration of progesterone induced a significant and prolonged rise in LH, restoring AG-blocked ovulation in all hens treated (n = 6). Injections of testosterone restored LH release in all hens and ovulation in 2 of 7 hens treated. Three of 7 hens ovulated in response to the corticosterone injection. A preovulatory rise in LH was not observed, indicating that corticosterone may exert its ovulation-inducing effect directly on the mature follicle. Estradiol-17 beta did not restore LH release or ovulation in any of the hens treated with AG.     

Mechanism of delayed ovulation in a vespertilionid bat, scotophilus heathi: role of gonadotropin, insulin, and insulin-like growth factor-1

The aim of this study was to evaluate the effects of luteinizing hormone (LH), follicle-stimulating hormone (FSH), insulin, and insulin-like growth factor-1 (IGF-1) on ovarian androstenedione synthesis to understand the mechanism responsible for delayed ovulation in Scotophilus heathi. We found that LH stimulated a dose-dependent increase in androstenedione synthesis by the ovary in vitro. This study also showed a clear seasonal variation in the ability of the ovary to produce androstenedione in vitro in response to LH and FSH stimulation. In response to LH and FSH, maximum quantities of androstenedione were produced during recrudescence in November. The same doses of gonadotropins during the preovulatory period in February stimulated comparatively low androstenedione secretion by the ovary. On the basis of these data, we suggest that in S. heathi, ovarian responsiveness to LH and FSH peaks during recrudescence. This study also showed a seasonal variation in the effects of insulin and IGF-1 on ovarian androstenedione production in vitro. Peak ovarian responsiveness to insulin and IGF-1 was observed during quiescence in September. It is hypothesized that increased insulin/IGF-1 sensitivity during September may be responsible for increased responsiveness to LH. Increased LH release, if coincident with the period of enhanced ovarian responsiveness to LH, may result in the excessive androstenedione production responsible for delayed ovulation in S. heathi.     

Temporal relationships among LH, estradiol, and follicle vascularization preceding the first compared with later ovulations during the year in mares

Diameter of the preovulatory follicle, plasma concentrations of LH and estradiol, and vascularization of the follicle wall, based on color-Doppler signals, were characterized in 40 pony mares for 6 days preceding ovulation (Days -6 to -1; preovulatory period). Comparisons between the preovulatory periods preceding the first compared with a later ovulation during the year were used to study the relationships between LH and estradiol and between vascularization and estradiol. Diameter of the preovulatory follicle was greater (P<0.02) and concentration of LH was less (P<0.02) during the first preovulatory period, whereas concentration of estradiol was not different between the first and second preovulatory periods. Vascularized area (cm(2)) of the follicle wall increased at a reduced rate during the first preovulatory period, as indicated by an interaction (P<0.03) between day and group. Vascularized area was similar between the preovulatory groups on Day -6, and a reduced rate of increase resulted in a lesser (P<0.001) area on Day -1 before the first ovulation (1.4+/-0.1cm(2)) than before a later ovulation (2.2+/-0.2 cm(2)). Results demonstrated that follicle vascularization and the LH surge were attenuated preceding the first ovulation of the year with no indication that estradiol was involved in the differences between the first and later ovulations.     

Time of ovarian follicular recruitment in cyclic pony mares

An experiment was carried out on pony mares to establish the time of the oestrous cycle at which ovarian follicles are recruited for ovulation. In one group (n=7), the cycle was interrupted at the preovulatory stage by removing the preovulatory follicle; in another group (n=13) the cycle was interrupted at day 6 of the luteal phase by inducing luteolysis with a prostaglandin injection (PG). In a subgroup (n=7) of those given PG, the ovary not bearing the corpus luteum was removed at the time of injection. A further group (n=6) served as surgical controls. The interval to the next ovulation and blood concentrations of FSH were observed. Anaesthesia alone induced in preovulatory mares was followed by normal ovulation 2.5+/-1 days later. Removal of the preovulatory follicle delayed the next ovulation (14.6+/-2.1 days; P < 0.01). Following PG injection, the interval to ovulation was similar regardless of whether an ovary was removed (12.8+/-4.3 days) or not (10+/-4.1 days). This similarity occurred despite a large and prolonged rise in plasma FSH levels that occurred only in the hemiovariectomized group. In addition, the intervals found after PG injection did not differ from those found after ablation of the preovulatory follicle. These observations indicate that 1) in the presence of the early active corpus luteum or dominant follicle, follicles grow to a similar stage of development; 2) recruitment of the follicle due to ovulation occurs 12 to 14 days before ovulation; 3) limiting new follicular growth to one ovary does not affect the time course to ovulation; and 4) prolonged high FSH levels do not alter the time course or ovulation rate.     

Ovulatory response, and plasma concentrations of luteinizing hormone and progesterone following administration of synthetic mammalian or chicken luteinizing hormone-releasing hormone relative to the first or second ovulation in the sequence of the domestic hen

Experiments were conducted to investigate hypophyseal and follicular competency at two distinct stages of the hen's egg laying sequence: 1) 14 h prior to the first (C1) ovulation of a sequence (27 h following the previous ovulation); and 2) 14 h prior to the second (C2) ovulation of a sequence (13 h following the previous ovulation). When a single dose of mammalian luteinizing hormone-releasing hormone (mLHRH) or chicken luteinizing hormone-releasing hormone (cLHRH) was injected 14 h prior to a C1 ovulation, premature ovulation was induced in 19 of 20 hens. In contrast, ovulation was premature in only 1 of 20 hens when mLHRH or cLHRH was injected 14 h prior to a C2 ovulation. There was no difference between the two stages of the sequence in the amount of luteinizing hormone (LH) released for up to 60 min following a single i.v. injection of 20 micrograms mLHRH. However, only prior to a C1 ovulation did LH levels further increase to reach preovulatory concentrations. By contrast, progesterone (P4) concentrations were increased within the first 60 min to a lesser extent in hens injected prior to a C2 ovulation compared to a C1 ovulation. In C2-injected birds, P4 fell to levels that were not different from vehicle-injected controls by 45 to 60 min following injection, whereas P4 secretion was maintained in hens injected prior to a C1 ovulation. We suggest that the lack of sustained LH secretion following treatment with either species of LHRH 14 h prior to a C2 ovulation is related to follicular immaturity with respect to ability to produce and secrete P4. At the dosage administered, there was no difference in the ability of mLHRH compared to cLHRH to release LH at either stage of the sequence. Finally, two successive injections of mLHRH at 14 and 13 h prior to a C2 ovulation induced premature ovulation in 6 of 11 hens. It is suggested that LH, and possibly P4, exerts a priming effect on the largest preovulatory follicle to initiate fully potentiated P4 production and secretion.     

Evidence against a role of prolactin in the timing of ovulation in the turkey

Two separate experiments in which blood was sampled at 2-h intervals from turkeys hens failed to show a significant change in plasma prolactin (Prl) concentrations in relation to the preovulatory surge of luteinizing hormone (LH) for the first (C1) ovulation of a sequence. Intravenous injection of 125 IU of ovine Prl (NIH-P-S10) or of 1 or 2 ml of antiserum to turkey Prl at varying intervals before C1 ovulation had no effect on the timing or incidence of C1 ovulation. However, injection of Prl before C1 ovulation tended to inhibit ovulation of the second (C2) egg of the sequence, while injection of antiserum to Prl before C1 ovulation tended to either advance or inhibit C2 ovulation. Possibly, the effects of Prl and Prl antiserum on C2 ovulation reflect interference with maturation of the C2 ovarian follicle rather than interference with neuroendocrine processes that regulate the timing of the preovulatory surge of LH. The data for C1 ovulation argue against a change in circulating levels of Prl as a factor in the timing of the preovulatory surge of LH.     

Adrenal gland involvement in synchronizing the preovulatory release of LH in rats.

In this study we have demonstrated that acute adrenalectomy (1000 hr proestrus) has no effect on the release of LH on proestrous afternoon. However, chronic adrenalectomy results in the loss of some factor responsible for synchronizing the preovulatory LH surge. Since this investigator has shown previously (15) that progesterone can influence the timing of LH release in ovariectomized and ovariectomized-adrenalectomized animals, it is most likely that adrenal progesterone is involved in synchronizing this event.     

Regulation of the follicular hierarchy and ovulation

Studies are discussed which investigate the regulation of follicular maturation and the ovulation sequence of the domestic hen. The number of FSH receptors of ovarian granulosa cells decreases as the follicle matures, and this decrease in receptor number is paralleled by a gradual loss of FSH-stimulable adenylyl cyclase (AC) activity. By contrast, LH-stimulable AC activity increases as the follicle progresses through the hierarchy. In addition, FSH stimulates progesterone secretion by granulosa cells of the smaller preovulatory follicles, whereas these cells are only minimally responsive to LH. These data suggest that the maturation of less mature (smaller) follicles is primarily controlled by FSH, while LH may serve primarily as the ovulation-inducing hormone. The ability of LH to stimulate progesterone release and induce premature ovulation is dependent upon the stage of the sequence. Injection of ovine LH 12 hr prior to ovulation of the first (C1) egg of the sequence induces fully potentiated preovulatory plasma progesterone surges and 100% premature ovulation, whereas injection prior to the second (C2) ovulation of the sequence fails to stimulate prolonged progesterone release and induces premature ovulation in less than 50% of injected hens. These results are consistent with data obtained in vitro which suggest that granulosa cells obtained 12 hr prior to a C1 ovulation secrete more progesterone in response to chicken LH compared to those obtained 12 hr prior to the C2 ovulation. These data are discussed in terms of the ovary's ability to act as a regulator of the ovulatory cycle.     

Synchronization of estrus and ovulation and associated endocrine changes in Bos indicus cows

The effects of 4 estrus synchronization treatments on intervals to and synchrony of estrus and ovulation, on timing of the preovulatory LH surge and associated changes in plasma progesterone, LH, FSH, and 17beta-estradiol (E(2)) were investigated in 48 Bos indicus cows. Treatment 1 consisted of 2 injections of PGF(2alpha) 14 d apart (n = 12); Treatment 2 of a subcutaneous 3-mg norgestomet implant and an intramuscular injection of 3 mg of norgestomet and 5 mg estradiol valerate, with the implant removed 10 d later (n = 12; norgestomet-estradiol); Treatment 3 of norgestomet-estradiol, with a subcutaneous injection of PMSG given at time of implant removal (Day 10; n = 12); and Treatment 4 of norgestomet implant (as for Treatments 2 and 3) inserted for 10 d, with an intramuscular injection of PGF(2alpha) given at the time of implant removal (n = 12). The experiment was conducted in 2 replicates (24 cows/replicate, 6 cows/group). Estrus, ovulation and timing of the preovulatory surge of LH varied less in cows treated with norgestomet-estradiol and PMSG than in cows in Treatments 1 and 4 (P < 0.008). Treatment with PMSG reduced variation in ovulation times and timing of the LH surge in cows treated with norgestomet-estradiol (P < 0.02). Concentrations of E(2) were higher in cows in Treatments 2 and 3 on the final day of treatment and at about 6 h post ovulation compared with cows in Treatments 1 and 4 (P < 0.05). Different methods for synchronizing estrus did not alter sequential endocrine and behavioral changes in relation to the timing of the LH peak, and the results were consistent with current recommendations for insemination times in Bos taurus cattle.     

Local delivery of angiopoietin-2 into the preovulatory follicle terminates the menstrual cycle in rhesus monkeys

The angiopoietin (ANGPT)-receptor (TEK) system plays a crucial role in blood vessel formation and stability. Because the endogenous agonist ANGPT1, antagonist ANGPT2, and TEK are expressed in the primate ovary, experiments were designed to investigate their role at a critical time during tissue remodeling/ angiogenesis in the menstrual cycle (i.e., at midcycle during maturation, ovulation, and luteinization of the dominant follicle). Either vehicle, 20 microg of ANGPT1, 2 microg of ANGPT2 (low-dose), or 20 microg of ANGPT2 (high-dose) was injected directly into the preovulatory follicle of monkeys around the day (-1 to 0) of the midcycle estradiol (E2)/LH peak. Ovaries were evaluated on Day 3 postinjection for follicle rupture, and serum samples were analyzed for levels of E2 and progesterone. Similar to controls, ANGPT1 treatment was followed by ovulation, and elevated progesterone levels during the luteal phase. In contrast, high-dose ANGPT2 treatment prevented follicle rupture, and progesterone levels never rose above baseline in the subsequent 12 days. However, an E2 peak typically occurred 12 days postinjection. Laparoscopy detected a preovulatory follicle on the contralateral (noninjected) ovary. Progesterone levels subsequently increased above baseline in these animals. Thus, exogenous ANGPT2 disrupted maturation of the preovulatory follicle, preventing its ovulation and conversion into the corpus luteum. ANGPT antagonism eliminated the dominant structure, thereby resetting the ovarian cycle, with selection and maturation of the next preovulatory follicle occurring in a timely manner. The data are consistent with a critical role of the ANGPT-TIE1/TEK system in the ovary, notably at the late stages of follicle maturation during the menstrual cycle.     

Prevention of continuous light-induced anovulation in rats by early exposure to continuous light

Continuous illumination (LL) beginning at 22 days of age caused precocious puberty followed by persistent estrus with anovulation in female offspring originating from mother rats exposed to a 14L:10D light-dark cycle prior to and during pregnancy. However, LL had no deleterious effect on reproductive cycles of offspring reared in LL and originating from mothers exposed to LL prior to and during pregnancy. These rats had a normal onset of puberty in LL, a normal 4-day estrous cycle, a periodic rise of plasma estrogen prior to the periodic appearance of the preovulatory luteinizing hormone (LH) surge, and spontaneous ovulation in LL continued until at least 300 days of age. Also, the female offspring of these rats showed a similar resistance to the deleterious effects of LL on cyclic ovulation. These results support the following interpretation: 1) offspring from mother rats exposed to LL prior to and during pregnancy become insensitive to the deleterious effects of LL on cyclic ovulation, 2) neural elements controlling cyclic release of LH are not totally photoperiod (14L:10D)-dependent, and 3) in the absence of daily 14L:10D signals, an endogenous clock, possibly timed by daily laboratory signals (temperature, noise, taking of vaginal smears), may provide time cues for cyclic LH release.     

Agouti-related protein has an inhibitory paracrine role in the rat adrenal gland

alpha-Melanocyte-stimulating-hormone (alpha-MSH) is an agonist at the melanocortin 3 receptor (MC3-R) and melanocortin 4 receptor (MC4-R). alpha-MSH stimulates corticosterone release from rat adrenal glomerulosa cells in vitro. Agouti-related protein (AgRP) an endogenous antagonist at the MC3-R and MC4-R, is expressed in the adrenal gland. We investigated the expression of the MC3-R and MC4-R and the role of AgRP in the adrenal gland. MC3-R and MC4-R expression was detected in rat adrenal gland using RT-PCR. The effect of AgRP on alpha-MSH-induced corticosterone release was investigated using dispersed rat adrenal glomerulosa cells. AgRP administered alone did not affect corticosterone release, but co-administration of AgRP and alpha-MSH attenuated alpha-MSH-induced corticosterone release. To investigate glucocorticoid feedback, adrenal AgRP expression was compared in rats treated with dexamethasone to controls. AgRP mRNA was increased in rats treated with dexamethasone treatment compared to controls. Our findings demonstrate that adrenal AgRP mRNA is regulated by glucocorticoids. AgRP acting via the MC3-R or MC4-R may have an inhibitory paracrine role, blocking alpha-MSH-induced corticosterone secretion.     

Adenylyl cyclase system of the small preovulatory follicles of the domestic hen: responsiveness to follicle-stimulating hormone and luteinizing hormone

The purpose of this study was to determine if the granulosa cells of the small preovulatory follicles of the domestic hen are a target tissue for follicle-stimulating hormone (FSH). The third largest (F3), fourth largest (F4), and fifth largest (F5) follicles were removed from hens at 20, 12, 6 and 2 h before ovulation of the F1 follicle. Basal, FSH- and luteinizing hormone (LH)-stimulable adenylyl cyclase (AC) activities were measured in the granulosa cells. Isolated granulosa cells of the F5 follicle, obtained 20 h before ovulation of the F1 follicle, were incubated with ovine (o) or turkey (t) FSH and progesterone (P4) was assayed in the medium. Basal AC activity was similar for F5, F4 and F3 granulosa cells except for an increase (P less than 0.01) in F3 follicles removed 2 h before ovulation of the F1 follicle. The FSH-stimulable AC activity of F5, F4 and F3 granulosa cells was elevated over basal (P less than 0.01). The greatest responsiveness was seen in the F5 follicle and the least in the F3 follicle. LH-stimulable AC activity was absent in the F5 follicle but present in the F4 and F3 follicles with the greater responsiveness in the F3 follicle. Isolated F5 granulosa cells secreted significant amounts of P4 in response to oFSH and tFSH. The data indicate that: 1) FSH stimulates the AC system of granulosa cells of the smaller preovulatory follicles (F5 greater than F4 greater than F3) while LH stimulates the AC system of granulosa cells of the larger follicles (F3 greater than F4), and 2) FSH promotes P4 production by granulosa cells of F5 follicles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Concentrations of steroids in the utero-ovarian vein blood,serially collected from the two sides of individual baboons,during the follicullar phase

The purpose of this study was to determine and compare the follicular phase steroid hormone secretion into the utero-ovarian vein by the ovary with a dominant follicle and the contralateral ovary in the same baboon. Serial utero-ovarian vein blood from both sides was collected in 25 baboons by the use of a laparoscope on alternate days, starting on day 1 or 3 of the cycle and continuing through 2 to 3 days post-ovulation. Approximately 3–4 days before the day of expected ovulation, samples were collected at 8-hr intervals. Steroids estradiol (E₂) and progesterone (P) were measured in all utero-ovarian vein plasma by radioimmunoassay. In the peripheral plasma, E₂, P, LH, and FSH measurements were carried out. Concentrations of steroids were significantly higher on the side of the ovulating ovary by day 5 before ovulation. Individual plots however, indicated that some baboons may establish the dominant side as early as day 11 before ovulation. The preovulatory gonadotropins had a differential effect on the two ovaries. For example, E₂ values on the ovulatory side ovary declined after increases in LH/FSH, whereas on the contralateral side these values had increased. Both sides showed increases in the level of P with the increases in LH. The mean interval from E₂ peak to LH peak was 24 hrs and LH peak to ovulation was 24 hrs.     

Nonluteal source of lordosis-promoting progesterone secretion in guinea pigs

Prepubertal (21-24 days of age), intact female guinea pigs treated sequentially with estradiol benzoate and LH or FSH displayed lordosis behavior. The gonadotropins apparently caused release of progesterone from the ovaries, because lordosis behavior in guinea pigs is activated by sequential action of estrogen and progesterone. These data demonstrate that immature ovaries, completely devoid of corpus luteum tissue, are capable of secreting behaviorally significant concentrations of progesterone when stimulated by gonadotropins. Therefore, the luteal compartment of the guinea pig ovary is not essential for the preovulatory surges of progesterone that coincide with expression of lordosis behavior in adulthood. Likely candidates for sources of preovulatory progesterone in prepubertal females are antral follicle and interstitial gland tissue.     

The differential effect of atrazine on luteinizing hormone release in adrenalectomized adult female Wistar rats

High doses of atrazine (ATR), administered for 4 days, suppress luteinizing hormone (LH) release and increase adrenal hormones levels. Considering the known inhibitory effects of adrenal hormones on the hypothalamo-pituitary-gonadal axis, we investigated the possible role the adrenal gland has in mediating ATR inhibition of LH release. To determine the extant and duration of adrenal activation, ovariectomized Wistar rats were given a single dose of ATR (0, 50, or 200 mg/kg), and corticosterone (CORT) levels were assayed at multiple time points posttreatment. CORT levels were increased within 20 min and remained elevated over 12 h postgavage in 200-mg/kg animals. To determine the effects of adrenalectomy on ATR inhibition of the LH surge and pulsatile LH release, adrenalectomized (ADX) or sham-operated ovariectomized rats were treated for 4 days with ATR (0, 10, 100, or 200 mg/kg), and an LH surge was induced with hormone priming. In the afternoon following the last dose of ATR, blood was sampled hourly for 9 h. Another cohort of ovariectomized rats was examined for pulsatile patterns of LH secretion after ATR (0, 50, or 200 mg/kg) and sampled every 5 min for 3 h. ADX had no effect on ATR inhibition of the LH surge but prevented the ATR disruption of pulsatile LH release. These data indicate that ATR selectively affects the LH pulse generator through alterations in adrenal hormone secretion. Adrenal activation does not play a role in ATR's suppression of the LH surge, and therefore ATR may work centrally to alter the preovulatory LH surge in female rats.     

Effect of the growth hormone-secreting tumor StW5 on pituitary and adrenal gland function in rats

A growth hormone-secreting tumor (StW5 was implanted into male rats and resulted in a tripling of adrenal weight concomitant with a 30% decrement in pituitary weight. Plasma concentrations of corticosterone in tumor-bearing (TB) rats were significantly elevated at rest or after ACTH injections or the stress of either anesthesia. The rise in plasma concentrations of corticosterone was due mainly to the large increment in adrenal size although a significant increase in adrenal responsiveness to ACTH was demonstrated in vitro. In addition, plasma corticosterone concentrations were higher in TB rats despite both a doubling of the blood volume and a 50% increase in liver capacity to metabolize corticosterone. Pituitary ACTH content was significantly lower in TB rats, but these pituitary glands could still release near-normal quantities of ACTH as shown both by in vitro incubations and adrenal corticosterone output following ether stress.     

Ultrasonic evaluation of the preovulatory follicle in the mare

Ultrasonically visible characteristics of preovulatory follicles in mares which single ovulated were studied daily for 79 preovulatory periods in 40 mares. The preovulatory follicle became the largest follicle in the ovary from which ovulation later occurred six or more days before ovulation in 65 of 79 (82%) preovulatory periods; the mean was day -7 (range, day -14 to day -4). The increase in mean diameter of the preovulatory follicle was linear (R(2)=99.5%) over day -7 (29.4 +/- 0.8 mm) to day -1 (45.2 +/- 0.5 mm; growth rate, 2.7 mm/day). Follicles which double-ovulated were smaller (P<0.05) on day -1 (36 +/- 1.6 mm; n=12 follicles). Preovulatory follicles exhibited a pronounced change in shape from a spherical to a conical or pear-shaped structure in 84% of the preovulatory periods. Remaining follicles retained a spherical shape. Scores representing thickness of the follicular wall increased (P<0.05) as the interval to ovulation decreased. There was no significant difference among days in mean gray-scale value of the follicular wall or in echogenicity of the follicular fluid. Although diameter and shape of the follicle and thickness of the follicular wall changed during the preovulatory period, no reliable ultrasonically visible predictor of impending ovulation was found.     

模拟高原低氧对新生大鼠肾上腺皮质功能发育的影晌

本文探讨新生大鼠肾上腺皮质对高原低氧的应答及模拟高原低氧对其功能发育的影响。结果表明,当不同日龄大鼠暴露于５ｋｍ及７ｋｍ海拔２４ｈ,７ｄ、１４ｄ龄大鼠肾上腺皮质无明显应答反应。２１ｄ及２８ｄ龄大鼠肾上腺皮质酮水平随海拔增高而增加,血浆皮质酮表现为抑制作用。当１ｄ龄新生大鼠在５ｋｍ海拔高度发育３ｄ和７ｄ,其肾上腺皮质功能无异于正常发育大鼠;但发育１４ｄ、２１ｄ及２８ｄ,其血液及肾上腺中皮质酮含量均明显低于对照组,肾上腺皮质功能发育严重受抑     

Inhibitory effect of serotonin on ovulation in the domestic fowl, Gallus domesticus

Serotonin (5-HT) treatment (20 mg/kg) of White Leghorn layers 8 h before expected time of egg release from the ovary inhibited ovulation. This inhibitory effect was overcome by LH administration. Progesterone injection 14 h before anticipated ovulation caused premature ovulation. 5-HT injected 15 or 60 min before or after progesterone administration inhibited this ovulation. Non-significant inhibition (P < 0.05) of ovulation resulted when 5-HT was injected 120 or 180 min apart from progesterone administration. Results from these experiments suggest that the 5-HT effect on ovulation is not mediated through direct effect on the ovary but probably by inhibiting the release of LH.