1 Department of Animal
Reproduction, The physiological
importance of gonadal hormones in feedback control of gonadotropin
secretion during the estrous cycle in golden hamsters was investigated
with immunoneutralization methods. Anti-inhibin serum (inhibin-AS)
treatment always induced a drastic increase in follicle-stimulating
hormone (FSH) secretion and occasionally raised luteinizing hormone
(LH) secretion. Anti-estradiol-17
immunoneutralization; follicle-stimulating hormone; luteinizing
hormone; estrous cycle; feedback
IT IS WELL KNOWN that gonadectomy causes the increase
in plasma concentrations of gonadotropins in many species. In the
golden hamster (Mesocricetus
auratus), plasma concentrations of
follicle-stimulating hormone (FSH) and luteinizing hormone (LH)
increase after ovariectomy (35), and gonadal steroid hormones have been
thought to be primary factors in the regulation of gonadotropins (4,
11, 35, 36) in this species. It has been established that inhibin is a
major inhibiting factor for FSH secretion in several species (6, 28).
Recently, we demonstrated that plasma concentrations of inhibin
fluctuate throughout the estrous cycle in the hamster and that the
pattern of circulating inhibin shows an inverse relationship to that of
FSH, suggesting that inhibin is the primary regulator of FSH secretion
in the hamster as well as in other species (21). Administration of
antiserum against inhibin in cyclic hamsters (20) and cyclic rats (1,
29) causes a dramatic increase in plasma FSH and in the spontaneous
ovulation rate on day
1 of the next estrous cycle in the
hamster. These observations suggest that inhibin regulates ovulation
rate in these species by controlling secretion of FSH. However, it is
still unclear as to how effectively endogenous inhibin regulates FSH
secretion during the estrous cycle in the hamster, as plasma inhibin
fluctuates during the ovarian cycle.
In the present study, we have investigated the role of endogenous
inhibin, estradiol-17 Animals
ABSTRACT
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
serum (estradiol-AS) treatment
increased LH secretion typically. Although estradiol-AS elevated FSH
secretion occasionally, the elevation was much less than that by
inhibin-AS. Plasma FSH reached ovariectomized levels by a synergistic
effect of both antisera. Elevated plasma LH with both antisera was much
less pronounced than in ovariectomized animals. Plasma LH increased
dramatically to the levels in the ovariectomized group when antibody
against progesterone (progesterone-AB) was given together with
inhibin-AS and estradiol-AS, although progesterone-monoclonal
antibody alone did not alter plasma gonadotropin levels.
These results indicate that in hamsters FSH secretion is mainly
regulated by inhibin and LH secretion is regulated by estradiol-17
and progesterone during the estrous cycle.
INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
, and progesterone in the release of
gonadotropins by means of immunoneutralization at various stages of the
estrous cycle of the hamster.
MATERIALS AND METHODS
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
Antiserum Against Estradiol-17 or Against Inhibin
Monoclonal Antibody to Progesterone
Monoclonal antibody to progesterone (progesterone-AB) used in this study was obtained as described previously (17). In brief, BALB/c mice were hyperimmunized with progesterone-11Effects of Inhibin-AS, Estradiol-AS, or the Combined Treatment on Gonadotropin Secretion at Various Stages of the Estrous Cycle
In this experiment, effects of immunoneutralization against inhibin and/or estradiol on gonadotropin secretion were investigated at five stages of ovarian status, based on previous studies (13-16, 21, 22). The five stages of ovarian status were as follows: 1) at 1100 on day 1, the ovary manifests no healthy antral follicles, but several small or medium-sized preantral follicles and newly formed corpora lutea are present. Plasma concentrations of inhibin and estradiol-17Antiserum or control serum was injected (iv) once, under light ether
anesthesia, into individual animals via the jugular vein at 1100 or
2300 on day
1, at 1100 on
days
2 and
3, or at 0500 on
day
4. Each injection volume was adjusted
to 200 µl; for example, 100 µl of estradiol-AS and 100 µl of
control serum were administered in the estradiol-AS treatment group and
200 µl of control serum were injected in the control group. Each
group of animals was killed by decapitation at 6 or 12 h after the
serum injection, and trunk blood samples were collected in heparinized
centrifuge tubes. Blood samples were centrifuged
immediately at 1,700 g for 15 min at
4°C, and plasma was separated and stored at 20°C until assayed for FSH and LH.
A bilateral ovariectomy was performed on animals to deprive them of the
ovarian factors under light ether anesthesia at 1100 or 2300 on
day
1, at 1100 on
days
2 and
3, or at 0500 on
day
4. Each group of animals
was killed by decapitation 6 or 12 h after the operation, and trunk
blood samples were collected in heparinized centrifuge tubes. Plasma
samples were obtained as described above and stored at 20°C
until assayed for FSH and LH.
Effect of Progesterone-AB on the Secretion of Gonadotropins
Various doses of progesterone-AB (0.0625-1.0 mg progesterone-AB/200 µl PBS) were given to individual animals at 1100 on day 2 of the estrous cycle when plasma progesterone began to increase in the estrous cycle of the intact hamster (2, 21, 27). Each group of animals was killed by decapitation at 6 and 12 h after treatment, and trunk blood samples were collected. Plasma samples were obtained after centrifugation and stored atEffect of Combined Treatment with Inhibin-AS, Estradiol-AS, and Progesterone-AB on the Secretion of Gonadotropins
Combined treatment with both 100 µl inhibin-AS and 100 µl estradiol-AS or combined administration of 100 µl inhibin-AS, 100 µl estradiol-AS, and 1 mg progesterone-AB was undertaken at 1100 on day 2 of the estrous cycle. Plasma samples were collected at 6 and 12 h after treatment as described previously and stored atRIAs for Gonadotropins
Plasma concentrations of FSH and LH were measured using National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) RIA kits for rat FSH and LH as described previously (3). Iodinated preparations were rat FSH-I-7 and LH-I-8. The antisera used were anti-rat FSH-S-11 and anti-rat LH-S-10. Results were expressed in terms of NIDDK rat FSH-RP-2 and rat LH-RP-2. The intra- and interassay coefficients of variation were 4.4 and 14.6% for FSH and 8.9 and 6.7% for LH, respectively.Statistics
The values of plasma gonadotropin concentrations were expressed as means ± SE of five animals. The comparison of two means was made by the Student's t-test or the Cochran-Cox test. The comparison among treatment groups was performed by one-way ANOVA, followed by Duncan's multiple-range test (32). When there was heterogeneity of variance, the logarithmic transformation was carried out before ANOVA. Values of P < 0.05 were considered to be statistically significant. ![]() |
RESULTS |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Changes in Plasma Concentrations of FSH and LH After Treatment with Inhibin-AS, Estradiol-AS, or Both at Various Stages of the Estrous Cycle
Treatment at 1100 on day 1. Plasma concentrations of FSH after administration of inhibin-AS or combined treatment were significantly higher than in controls (Fig. 1, A and F). Plasma FSH after cotreatment with both inhibin-AS and estradiol-AS was increased further over that with injection of inhibin-AS alone; and the concentrations after combined treatment were similar to those observed in the ovariectomized group. On the other hand, treatment with estradiol-AS alone had little effect on plasma FSH. Slightly but significantly increased plasma FSH was noted 12 h after treatment in the group given estradiol-AS.
|
Plasma concentrations of LH were increased significantly 6 h after administration of estradiol-AS alone or combined treatment with inhibin-AS and estradiol-AS compared with controls, and they were similar to the levels in ovariectomized animals. However, the LH concentrations 12 h after treatment were significantly lower than those in the ovariectomized group, and there was no significant difference between plasma concentrations of LH in the various treatment groups (estradiol-AS alone, inhibin-AS plus estradiol-AS, or control serum).
Treatment at 2300 on day 1. Plasma concentrations of FSH were increased significantly after treatment with inhibin-AS alone or inhibin-AS plus estradiol-AS compared with the controls (Fig. 1, B and G). Administration of inhibin-AS in combination with estradiol-AS increased plasma FSH to a level that was higher than that found in animals treated with inhibin-AS alone but similar to that observed in the ovariectomized group. Treatment with estradiol-AS led to a modest but significant increase in plasma FSH when measured 6 h after treatment; FSH returned to control levels thereafter.
No effect of any antisera on plasma concentrations of LH was noted in this experiment. Plasma concentrations of LH after ovariectomy were significantly higher than after any treatment. The effect on LH was more pronounced 6 h after the ovariectomy performed at 2300 on day 1 of the cycle than that performed at 1100 on the same day.
Treatment at 1100 on day 2. Plasma concentrations of FSH increased significantly after administration of inhibin-AS alone or after combined treatment (inhibin-AS plus estradiol-AS; Fig. 1, C and H). Cotreatment markedly raised concentrations of FSH when compared with inhibin-AS alone; the values after treatment with both antisera were similar to those in the ovariectomized group 6 h after treatment. However, at 12 h after treatment, the ovariectomized group showed significantly higher levels of FSH than did the combined-treatment group.
Treatment with estradiol-AS as well as combined administration of inhibin-AS and estradiol AS caused a significant increase in plasma concentrations of LH compared with the controls. Even higher plasma LH levels were noted after combined treatment, compared with estradiol-AS alone; however, this increase was attenuated in comparison with levels in the ovariectomized group. The impact on LH was greater when ovariectomy was carried out at 1100 on day 2 compared with that performed at 2300 on day 1 of the estrous cycle.
Treatment at 1100 on day 3. Significant increases in plasma FSH were found in all experimental groups when compared with the controls (Fig. 1, D and I). However, the values in the estradiol-AS-treated group were much smaller than those in other groups. Although plasma FSH after combined treatment was not higher than in the group given inhibin-AS alone when measured at 6 h after administration, it was markedly elevated thereafter.
All forms of treatment resulted in significant increases in plasma LH levels. At 12 h after treatment, a further increase was observed in the cotreatment group and the values were comparable to those in the ovariectomized animals.
Treatment at 0500 on day 4. Plasma FSH increased significantly at 6 h after treatment with inhibin-AS or a combination of inhibin AS and estradiol-AS but not after the treatment with estradiol-AS alone (Fig. 1, E and J). Combined treatment caused a greater FSH rise than that after inhibin-AS injection, and the level corresponded to that found in the ovariectomized group.
Plasma concentrations of LH did not change at 6 h after any antiserum treatment but were elevated by ovariectomy. At 12 h after treatment (except for inhibin-AS treated group), the surge levels of LH in the plasma declined significantly compared with the control levels. The impact of ovariectomy on plasma LH is less effective than that observed at 1100 on day 2 or 3.
Changes in Plasma Concentrations of FSH and LH After Treatment with Progesterone-AB at 1100 on Day 2
No alteration in plasma concentrations of FSH and LH was found after treatment with progesterone-AB, and their levels were similar to those after treatment with control serum (data not shown).Changes in Plasma Concentrations of FSH and LH After Combined Treatment with Inhibin-AS, Estradiol-AS, and Progesterone-AB at 1100 on Day 2
Treatment with a combination of inhibin-AS, estradiol-AS, and progesterone-AB caused a significant increase in plasma concentrations of FSH and LH compared with the controls; the increased FSH concentrations were slightly higher than those after combined treatment with inhibin-AS and estradiol-AS and were similar to those in the ovariectomized group (Fig. 2). Plasma LH after combined administration of inhibin-AS, estradiol-AS, and progesterone-AB was increased over that of combined administration of inhibin-AS and estradiol-AS, and the levels corresponded to those observed after ovariectomy.
|
![]() |
DISCUSSION |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
Immunoneutralization against inhibin caused a significant increase in the plasma concentrations of FSH at 6 and 12 h after treatment when compared with those in control animals. The elevated FSH levels after immunoneutralization against endogenous inhibin were similar to the second FSH surge levels found in our previous study (21). The FSH levels after treatment with inhibin-AS were higher at each point than those in animals treated with estradiol-AS (even though plasma concentrations of FSH were elevated over controls at some points by estradiol-AS treatment). Our previous reports (19, 20) showed that immunoneutralization of inhibin in the cyclic hamster on day 2 or 3 also caused an increase in plasma concentrations of FSH and superovulation on day 1 of the next estrous cycle. The present findings together with previous results suggest that circulating inhibin plays a major role in determining the number of developing follicles in the ovaries and regulates FSH secretion negatively to fix the species-specific ovulation rates in golden hamsters, as well as in rats (1, 29), cows (18), and sheep (23).
In the present study, the elevation rate in FSH concentrations in plasma after inhibin-AS treatment on the morning of day 1 was less than that after the treatment on other cycle days, compared with rats (1). The morning of day 1 is the time just after ovulation, when mature follicles (which are thought to be the main source of circulating inhibin) do not exist in the ovaries (14, 21). Therefore, we believe that plasma concentrations of FSH were already high because of low plasma concentrations of inhibin, indicating that the immunoneutralization against inhibin during this stage does not induce further elevation of plasma FSH.
The small stimulation of FSH secretion by immunoneutralization against
estradiol-17 was also observed on
day 1 or 3 but not on
day 2 or 4. This time the discrepancy in
results might come from the changing pattern in plasma concentrations
of estradiol-17
during the estrous cycle of hamsters. Based on our
previous report (21), plasma estradiol-17
enters a first incremental
phase from the morning of day
1 and a second incremental phase from the morning of day
3. On the other hand, it enters a
first decremental phase from the morning of
day 2 and a second decremental phase from the morning of
day
4. Plasma concentrations of inhibin
have already reached their zenith levels by the night of
day
1. Therefore, it may be
difficult to distinguish the effect of estradiol-AS itself given on
days
2 and
4 from that of decreased circulating estradiol-17
in the control group when FSH secretion is suppressed by high levels of plasma inhibin. A large dose of estradiol suppresses plasma concentrations of FSH in ovariectomized hamsters (4, 35, 36).
Estradiol inhibits the postcastration rise in FSH
-subunit mRNA in
the rat (10). Passive immunization of estradiol-17
causes the
elevation of plasma concentrations of FSH in rats (1) and sheep (24).
These reports also support our contention that estradiol-17
acts as
a negative regulator of FSH secretion.
In the present study, further increases were observed most of the time
in plasma concentrations of FSH in the animals treated with both
inhibin-AS and estradiol-AS, compared with those in animals treated
with inhibin-AS alone (as well as in a rat study with the same
antisera; Ref. 1). The amount of inhibin-AS used in the
present study is thought to be enough to cause maximal increment in
plasma FSH (20). These findings suggest that the action of
estradiol-17 on the suppression of FSH secretion may be different
from that of inhibin. Inhibin is generally thought to act on the
pituitary directly. On the other hand, it is thought that negative
effects of estradiol-17
act on hypothalamus rather than on pituitary
(7, 30, 31). Therefore, additive stimulation caused by inhibin-AS and
estradiol-AS is thought to be the mode of inhibin action, via
suppression of FSH production by the pituitary and the action of
estradiol-17
in suppression of gonadotropin-releasing hormone (GnRH)
secretion for the hypothalamus. It is also reported that
estradiol-17
directly regulates FSH secretion from the pituitary and
has the ability to suppress FSH secretion in the ovine pituitary cell
culture system (26). On the other hand, the levels of FSH after
treatment with both antisera were comparable to those after ovariectomy, suggesting that inhibin and estradiol-17
in the plasma
regulate FSH secretion negatively in the cyclic hamster.
Plasma concentrations of FSH 12 h after cotreatment with both antisera on day 3 were higher than those after ovariectomy, suggesting that ovarian factors that stimulate FSH secretion, such as activin, might play a small role in regulating the secretion of FSH during this time.
When estradiol-AS was administered to the cyclic hamster, plasma LH
increased in most of phases studied, compared with the respective
controls. As demonstrated in previous reports (4, 35, 36), the present
results indicate that circulating estradiol-17 is an important
negative regulator of basal LH secretion during the estrous cycle of
hamsters. In many cases in the present study, however, plasma
concentrations of LH after immunoneutralization against estradiol-17
were much lower than those after ovariectomy.
A synergistic effect on basal levels of LH was found when inhibin-AS was superimposed on estradiol-AS at 1100 on day 2 or 3 of the estrous cycle. In this case, inhibin-AS alone can also cause an increase in the basal plasma levels of LH. These observations suggest that circulating inhibin may act as a regulator of LH secretion, at least on days 2 and 3 of the estrous cycle. It is still arguable whether inhibin itself is involved in the secretion of LH in female rats. Rivier and Vale (29) demonstrated that circulating inhibin does not alter rat LH secretion by using antiserum against inhibin, whereas other studies (1, 5) show that endogenous inhibin suppresses LH secretion. Previous work (19, 20) also shows that immunoneutralization of inhibin on day 2 or 3 of the estrous cycle raises (temporally but significantly) plasma concentrations of LH in the cyclic hamster. These discrepancies may be related to the potency of antiserum used in each experiment. This consideration can be supported by our previous report (20) in which treatment with 50 µl or more, but not 25 µl or less, antiserum against inhibin caused an increase in plasma LH (although 12.5 µl of the same antiserum already led to a maximal increase in plasma concentrations of FSH). Farnworth et al. (9) demonstrated that purified bovine inhibin suppresses LH as well as FSH release with a rat pituitary cell culture system. Wang et al. (37) reported that purified bovine inhibin decreases the number of specific binding sites for GnRH on rat anterior pituitary cells in vitro. These findings suggest that inhibin appears to be a putative regulator of LH secretion in the cyclic hamster.
The present study suggests species differences in the stimulatory
effect of cotreatment with estradiol-AS and inhibin-AS on basal LH
secretion. The elevated levels of plasma LH after both antisera were
clearly lower than those after ovariectomy in the hamster, unlike the
rat (1). This suggests that the regulation of basal LH secretion in the
hamster is different from that in the rat. Although no effect was shown
by treatment with progesterone-AB alone on plasma concentrations of
gonadotropins, the levels after immunoneutralization against three
hormones (inhibin, estradiol-17, and progesterone) on the morning of
day 3 corresponded to those after ovariectomy. This observation suggests that
progesterone plays an important role as a negative regulator of basal
LH secretion in the hamster only when it acts in synergy with
estradiol-17
and inhibin. Vomachka and Greenwald (35, 36)
demonstrated that cotreatment with both estradiol and progesterone is
more effective in the suppression of the ovariectomy-induced elevation in plasma LH than treatment with either separately. In addition, Goodman and Karsch (12) showed the effect of ovarian steroids on the
profiles of the pulse secretion of LH, suggesting that estradiol-17
and progesterone could inhibit LH secretion by completely different
mechanisms through the modification of the pulse of GnRH. These results
may support the present findings that progesterone plays a cooperative
role in the presence of estradiol-17
on LH secretion. At the same
time, the synergistic effect of progesterone-AB on inhibin-AS and
estradiol-AS action was also found in the increase in FSH secretion,
although the effect was slight. This finding suggests that progesterone
would be a negative regulator of FSH secretion, as well as LH, in the
cyclic hamster.
Another species difference between the hamster and the rat was observed
in the gonadal regulation of LH secretion on
day
1. Plasma concentrations of LH
increased after ovariectomy on day 1 of the cycle in the hamster. On the
other hand, in the rat, elevation of concentrations of LH in the plasma
was not observed until at least 24 h after ovariectomy on the morning
of estrus (1), which corresponded with
day 1 in the hamster. One possibility of this species difference may come
from the difference between relative importance of estradiol-17 in
the hamster and the rat during this period. Plasma LH in the hamster
increased after treatment with estradiol-AS or cotreatment with
estradiol-AS and inhibin-AS on the morning of
day
1, but this increase in plasma LH
after treatment with estradiol-AS on the morning of estrus was not
observed in the rat (1).
In the present study, when estradiol-AS was given with or without
inhibin-AS, or ovariectomy was performed on the morning of
day
4, the LH surge was clearly diminished
compared with the control group. Although peak LH was lower, surge did
occur in all experimental groups on the afternoon of
day 4 as well as in the control group. This effect of ovariectomy agrees with
previous studies (11, 35), indicating that estradiol-17 on the
morning of day
4 is required to elicit a normal LH
surge. Norman and Spies (25) demonstrated that the diurnal LH elevation
via hypothalamus was induced 1 day after estrogen treatment. Therefore,
the present study also demonstrates that induction of the LH surge was
already established due to increased levels of plasma estradiol-17
until the morning of day
4.
In conclusion, plasma FSH concentrations in the hamster are primarily
regulated by circulating inhibin, and a synergistic effect of
estradiol-17 was noted during the estrous cycle of this species.
Circulating estradiol-17
mainly regulates plasma concentrations of
LH during the estrous cycle of the hamster, and circulating
progesterone may also play an important role in suppressing tonic
levels of LH in the hamster.
![]() |
ACKNOWLEDGEMENTS |
---|
We wish to express our gratitude to Dr. R. J. Hutz, Dept. of
Biological Sciences, University of Wisconsin Milwaukee, Milwaukee, WI,
for reading the original manuscript and for valuable suggestions. We
are also grateful to Dr. A. F. Parlow and the Rat Pituitary Hormone
Distribution Program, NIDDK, Bethesda, MD, for providing RIA materials
and to Dr. N. Ling, Neuroendocrine, San Diego, CA, for providing
[Tyr30]-inhibin (1-30).
![]() |
FOOTNOTES |
---|
This work was supported in part by Ciba-Geigy Foundation, a grant for Liberal Harmonious Research Promotion System from the Science and Technology Agency Japan, and US-Japan Cooperative Research Grant from the Japan Society for the Promotion of Science.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: K. Taya, Laboratory of Veterinary Physiology, Tokyo Univ. of Agriculture and Technology 3-5-8, Saiwai-cho, Fuchu, Tokyo 183-8509, Japan (E-mail: taya{at}cc.tuat.ac.jp).
Received 5 January 1999; accepted in final form 9 July 1999.
![]() |
REFERENCES |
---|
![]() ![]() ![]() ![]() ![]() ![]() ![]() |
---|
1.
Arai, K.,
G. Watanabe,
K. Taya,
and
S. Sasamoto.
Role of inhibin and estradiol in the regulation of follicle-stimulating hormone secretion during the estrous cycle of the rat.
Biol. Reprod.
55:
127-133,
1996[Abstract].
2.
Bast, J. D.
A comprehensive profile of peripheral progesterone levels in cyclic hamsters sequentially bled at 2-hr intervals.
Proc. Soc. Exp. Biol. Med.
162:
199-201,
1979.
3.
Bast, J. D.,
and
G. S. Greenwald.
Serum profiles of follicle-stimulating hormone, luteinizing hormone and prolactin during the estrous cycle in the hamster.
Endocrinology
94:
1295-1299,
1974[Medline].
4.
Chappel, S. C.,
R. L. Norman,
and
H. G. Spies.
Effects of estradiol on serum and pituitary gonadotropin concentrations during selective elevations of follicle stimulating hormone.
Biol. Reprod.
19:
159-166,
1978[Medline].
5.
Culler, M. D.,
and
A. Negro-Vilar.
Endogenous inhibin suppresses only basal follicle-stimulating hormone secretion but suppresses all parameters of pulsatile luteinizing hormone secretion in the diestrous female rat.
Endocrinology
124:
2944-2953,
1989[Abstract].
6.
DeJong, F. H.
Inhibin.
Physiol. Rev.
68:
555-607,
1988
7.
Drouin, J.,
L. Lagace,
and
F. Labrie.
Estradiol-induced increase of the LH responsiveness to LH releasing hormone (LHRH) in rat anterial pituitary cells in culture.
Endocrinology
99:
1477-1481,
1976[Abstract].
8.
Ellis, S. T.,
R. B. Heap,
A. R. Butchar,
V. Rider,
N. E. Richardson,
M.-W. Wang,
and
M. J. Taussig.
Efficacy and specificity of monoclonal antibodies to progesterone in preventing the establishment of pregnancy in the mouse.
J. Endocrinol.
118:
69-80,
1988[Abstract].
9.
Farnworth, P. G.,
D. M. Robertson,
D. M. de Kretser,
and
H. G. Burger.
Effects of 31 kilodalton bovine inhibin on follicle-stimulating hormone and luteinizing hormone in rat pituitary cells in vitro: action under basal conditions.
Endocrinology
122:
207-213,
1988[Abstract].
10.
Gharib, S. D.,
M. E. Wierman,
T. M. Badger,
and
W. W. Chin.
Sex steroid hormone regulation of follicle-stimulating hormone subunit messenger ribonucleic acid (mRNA) levels in the rat.
J. Clin. Invest.
80:
294-299,
1987[Medline].
11.
Goldman, B. D.,
V. B. Mahesh,
and
J. C. Porter.
The role of the ovary in control of cyclic LH release in the hamster, Mesocricetus auratus.
Biol. Reprod.
4:
57-65,
1971[Medline].
12.
Goodman, R. L.,
and
F. J. Karsch.
Pulsatile secretion of luteinizing hormone: differential suppression by ovarian steroids.
Endocrinology
107:
1286-1290,
1980[Abstract].
13.
Greenwald, G. S.
The effects of unilateral ovariectomy on follicular maturation in the hamster.
Endocrinology
66:
89-95,
1960.
14.
Greenwald, G. S.
Quantitative study of follicular development in the ovary of the intact or unilaterally ovariectomized hamster.
J. Reprod. Fertil.
2:
351-361,
1961.
15.
Greenwald, G. S.
Analysis of superovulation in the adult hamster.
Endocrinology
71:
378-389,
1962.
16.
Greenwald, G. S.
Temporal relationship between unilateral ovariectomy and the ovulatory response of the remaining ovary.
Endocrinology
71:
664-666,
1962.
17.
Greenwald, G. S.,
and
M.-W. Wang.
A monoclonal antibody to progesterone interrupts pregnancy in the hamster by curtailing secretion of the luteotropic complex of prolactin and follicle-stimulating hormone.
Endocrinology
129:
1735-1743,
1991[Abstract].
18.
Kaneko, H.,
Y. Nakanishi,
K. Taya,
H. Kishi,
G. Watanabe,
S. Sasamoto,
and
Y. Hasegawa.
Evidence that inhibin is an important factor in the regulation of FSH secretion during the mid-luteal phase in cows.
J. Endocrinol.
136:
35-41,
1993[Abstract].
19.
Kishi, H.,
T. Okada,
S. Kawazu,
M. Otsuka,
K. Taya,
G. Watanabe,
and
S. Sasamoto.
Effects of passive immunization against oestradiol-17 and inhibin on the secretion of gonadotropin in the cyclic golden hamster (Mesocricetus auratus).
Reprod. Fertil. Dev.
9:
447-453,
1997[Medline].
20.
Kishi, H.,
T. Okada,
M. Otsuka,
G. Watanabe,
K. Taya,
and
S. Sasamoto.
Induction of superovulation by immunoneutralization of endogenous inhibin through the increase in the secretion of follicle-stimulating hormone in the cyclic golden hamster.
J. Endocrinol.
151:
65-75,
1996[Abstract].
21.
Kishi, H.,
K. Taya,
G. Watanabe,
and
S. Sasamoto.
Follicular dynamics and secretion of inhibin and estradiol-17 during estrous cycle of the hamster.
J. Endocrinol.
146:
169-176,
1995[Abstract].
22.
Leavitt, W. W.,
C. R. Basom,
J. N. Bagwell,
and
G. C. Blaha.
Structure and function of the hamster corpus luteum during the estrous cycle.
Am. J. Anat.
136:
235-249,
1973[Medline].
23.
Mann, G. E.,
B. K. Campbell,
A. S. McNeilly,
and
D. T. Baird.
Passively immunizing ewes against inhibin during the luteal phase of the estrous cycle raises plasma concentration of FSH.
J. Endocrinol.
123:
383-391,
1989[Abstract].
24.
Mann, G. E.,
B. K. Campbell,
A. S. McNeilly,
and
D. T. Baird.
Effects of passively immunizing ewes against inhibin and estradiol during the follicular phase of the estrous cycle.
J. Endocrinol.
125:
417-424,
1990[Abstract].
25.
Norman, R. L.,
and
H. G. Spies.
Neural control of the estrogen-dependent twenty-four-hour periodicity of LH release in the golden hamster.
Endocrinology
95:
1367-1372,
1974[Medline].
26.
Philips, C. L.,
L.-W. Lin,
J. C. Wu,
K. Guzman,
A. Milsted,
and
W. L. Miller.
17-Estradiol and progesterone inhibit transcription of genes encoding the subunits of ovine follicle-stimulating hormone.
Mol. Endocrinol.
2:
641-649,
1988[Abstract].
27.
Ridley, K.,
and
G. S. Greenwald.
Progesterone levels measured every two hours in the cyclic hamster.
Proc. Soc. Exp. Biol. Med.
149:
10-12,
1975[Abstract].
28.
Rivier, C.,
H. Meunier,
V. Roberts,
and
W. Vale.
Inhibin: role and secretion in the rat.
Recent Prog. Horm. Res.
46:
231-259,
1990[Medline].
29.
Rivier, C.,
and
W. Vale.
Immunoneutralization of endogenous inhibin modifies hormone secretion and ovulation rate in the rat.
Endocrinology
125:
152-157,
1989[Abstract].
30.
Shupnik, M. A.,
S. D. Gharib,
and
W. W. Chin.
Divergent effects of estradiol on gonadotropin gene transcription in pituitary fragments.
Mol. Endocrinol.
3:
474-480,
1989[Abstract].
31.
Smith, P. F.,
L. S. Frawley,
and
J. D. Neil.
Detection of LH release from individual pituitary cells by reverse hemolytic plaque assay: estrogen increase the fraction of gonadotrope responding to GnRH.
Endocrinology
115:
2484-2486,
1984[Abstract].
32.
Steel, R. G. D.,
and
J. H. Torrie.
Principles and Procedures of Statistics. New York: McGraw-Hill, 1960, p. 107-109.
33.
Taussig, M. J.,
N. Brown,
S. Elli,
A. Holliman,
D. Peat,
N. Richardson,
R. B. Heap,
and
A. Feinstein.
Anti-idiotypic sera against monoclonal anti-progesterone antibodies: production in rabbits and rats and characterization of specificity.
Immunolog
y58:
445-452,
1986.
34.
Taya, K.,
and
S. Sasamoto.
Mechanisms responsible for suppression of FSH and LH during lactation in the rat.
J. Endocrinol.
129:
119-130,
1990.
35.
Vomachka, A. J.,
and
G. S. Greenwald.
Acute negative effects of ovarian steroid removal and replacement in the cyclic hamster.
Biol. Reprod.
19:
1040-1045,
1978[Medline].
36.
Vomachka, A. J.,
and
G. S. Greenwald.
Negative effects of ovarian steroids in the chronically ovariectomized hamster.
Biol. Reprod.
22:
1127-1135,
1980[Medline].
37.
Wang, Q. F.,
P. G. Farnworth,
J. K. Findlay,
and
H. G. Burger.
Effect of purified 31 k bovine inhibin on the specific binding of gonadotropin-releasing hormone to rat pituitary cells in culture.
Endocrinology
123:
2161-2166,
1988[Abstract].
38.
Wright, L. J.,
A. Feinstein,
R. B. Heap,
J. C. Saunders,
R. C. Bennet,
and
M.-W. Wang.
Progesterone monoclonal antibody blocks pregnancy in mice.
Nature
295:
415-417,
1982[Medline].
HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Visit Other APS Journals Online |