Abdominal vagotomy delays the onset of puberty and inhibits ovarian function in the female rat.
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Abdomen↗
Biomedical subjects
S S White
Publications and source records attributed to S S White.
Peripubertal decline in ovarian LHRH receptor content: characterization and distribution.
In the rat, ovarian LHRH receptor content, as measured by the binding of 125I-D-Ala6, Pro9-LHRH (A-LHRH) to ovarian membranes, decreases markedly during the days preceding the first preovulatory gonadotropin surge. The present study shows that the decrease in LHRH receptor number occurs exclusively in granulosa cells, and that the greatest rate of decline takes place between the juvenile period and the early proestrous phase of puberty. In contrast to granulosa cells, membranes prepared from ovarian tissues after removal of these cells demonstrated no significant change in LHRH binding capacity throughout puberty. Scatchard analysis of competition curves, constructed using membranes from whole ovaries, revealed that receptor affinity remains unchanged (Ka = 9 X 10(9) M-1) as the receptor number decreases. Kinetic binding studies demonstrated that LHRH binding to its receptor reaches equilibrium within 40 min and can be displaced by addition of unlabeled hormone. A kinetic estimate of receptor affinity provided values similar to those obtained by Scatchard analysis. Treatment of ovarian membranes with MgCl2 to uncover occupied binding sites results in more than 70% dissociation of bound labeled ligand. Dissociation of endogenous LHRH using this procedure resulted in some increase in available binding sites only in juvenile rats, but not in first proestrous or first estrous animals in which receptor content was low. The results demonstrate that the decline in ovarian LHRH receptors observed during peripubertal days is confined to granulosa cells, is not due to changes in receptor affinity, and represents a true loss of binding sites.
Animals↗
Pituitary LHRH receptors during puberty in the female rat: is the proestrous decline in receptor content due to occupancy?
As during the adult estrous cycle, the number of pituitary luteinizing hormone-releasing hormone (LHRH) receptors was found to increase prior to the first preovulatory surge of LH. Receptor content, as measured by the binding of the analog 125I-D-Ala6-Pro9-LHRH to pituitary membranes, declined markedly at the time of the first LH surge, remaining low during the first estrus and first diestrus. When pituitary membranes from animals undergoing an LH surge were incubated with MgCl2 to dissociate endogenously bound hormone, available binding sites were restored to pre-LH surge values. The increase in LHRH binding capacity was not related to an increase in receptor affinity, and it was not demonstrable in other pubertal phases. MgCl2 may have unmasked receptors made cryptic at the time of the LHRH-induced LH surge. Nevertheless, the results are compatible with the view that the proestrous decline in LHRH receptor content is, at least in part, due to occupancy of binding sites by endogenous hormone.
Animals↗
Changes in ovarian LHRH receptor content during the onset of puberty in the female rat.
LHRH and some of its analogs have been reported to exert inhibitory effects on ovarian function, seemingly following interaction of the neurohormone with specific, high affinity binding sites. The present experiments were undertaken to determine whether LHRH binding sites in the ovary undergo quantitative changes during the onset of puberty in the rat. Changes in LHRH receptor content were assessed by the binding of the stable LHRH analog, [D-Ala6, Pro9]-LHRH to ovarian membrane preparations. LHRH binding in prepubertal rats (anestrus, A) was 166 +/- 11 fmol/mg protein, declined gradually (to 127 +/- 14 fmol/mg protein) during the early proestrous (EP) phase of puberty--a time at which intrauterine fluid begins to accumulate and uterine weight increases more rapidly--and became even lower (75 +/- 4 fmol/mg protein) by 1300 h of the day of first proestrus (LP), prior to the initiation of the first gonadotropin surge. At the time of the surge (1600 h) binding was 70 +/- 3 fmol/mg protein. LHRH binding was minimal on the day of the first estrus (E) and increased slightly on diestrus (D). The results indicate that the ovarian steroidogenic activation that precedes the first surge of gonadotrophins in the rat is associated with a marked loss in ovarian LHRH receptor content and suggest that a reduction in LHRH inhibitory function within the ovary may be a contributing factor to the pubertal enhancement in ovarian secretory activity.
Animals↗
Activation of growth hormone short loop negative feedback delays puberty in the female rat.
Implantation of GH in the median eminence of the hypothalamus of 23-day-old female rats tonically inhibited serum GH levels throughout prepubertal development (days 23-36) and depressed GH diurnal pulsatile release. Puberty was significantly delayed in GH-deficient animals, a delay associated with a blunted in vitro ovarian steroidal responsiveness to gonadotropins (particularly estradiol) and a marked decrease in prepubertal uterine weight, as evaluated 4, 7, and 13 days after GH implantation. The prepubertal body weight increase was also depressed. Neither ovarian weight nor serum levels of LH, FSH, PRL, or TSH were consistently altered by the GH implant. In addition, evaluation of pulsatile PRL release in 33-day-old rats revealed no difference between control and GH-deficient animals. Ovarian LH receptor content was lower in GH-implanted rats than in controls, suggesting that a decrease in LH receptors may be one of the mechanisms by which a chronic decrease in serum gH depressed the prepubertal ovarian estradiol and, to a lesser extent, the progesterone response to gonadotropins. A direct ovarian site of action for GH was indicated by the results of experiments in which GH was administered to immature hypophysectomized estrogen-treated rats. The in vitro ovarian progesterone response of the GH-treated animals to both hCG and human FSH was distinctly increased by prior in vivo GH treatment. This effect of GH was not reproduced either by the in vivo administration of LH at a dose calculated by RIA to be contaminating the GH preparation or by FSH at a dose that induced a marked increase in aromatase activity in the same ovaries. GH treatment of hypophysectomized rats failed to affect either aromatase activity or hCG-induced estradiol release, indicating that GH does not directly facilitate the production of estradiol by the ovary. The fact that intact rats with GH implants did not actually show a decrease in the ovarian estradiol response to hCG but, rather, failed to show an increased response at the same time as control animals strongly suggests that ovarian maturation was delayed in GH-deficient rats. It is suggested that, in addition to PRL, GH may also play a role in the process of prepubertal reproductive development by enhancing the steroidal response of the ovary to gonadotropins.
Animals↗
Changes in ovarian luteinizing hormone and follicle-stimulating hormone receptor content and in gonadotropin-induced ornithine decarboxylase activity during prepubertal and pubertal development of the female rat.
Ovarian hCG and FSH receptor content was measured at different postnatal ages (days 4-32), at 4-day intervals, and expressed as counts per min 125I-labeled hormone bound/micrograms DNA. Specific FSH binding was minimal at day 4 and increased to a maximum at day 28, with the greatest rate of increase between day 4 and 16. hCG receptor content increased 6-fold between day 4 and 32, but contrasting with FSH, its greatest rate of increase occurred between day 16 and 28. The effectiveness of in vivo treatment with LH in inducing ovarian ornithine decarboxylase (ODC) activity, measured in 20,000 X g supernatants by the in vitro formation of 14CO2 from labeled ornithine, increased significantly during prepubertal development (days 21-33), paralleling the changes in hCG receptors. Ovarian hCG and FSH receptor content was also measured during the time of puberty. Specific hCG binding increased from anestrus (juvenile 32-day-old animals) to 1300 h of the first proestrus. The levels declined significantly by 1600 h of first proestrus and reached minimal values by the morning of estrus. Specific FSH binding also increased from anestrus to first proestrus, but to a much lesser degree, the levels showing only minor fluctuations during the rest of the cycle. hCG receptors measured in granulosa cells during puberty increased to an even greater extent than in the whole ovary; binding exhibited an 8-fold increase from anestrus to 1300 h of first proestrus and then declined to much lower values on estrus and the first diestrus. The capacity of LH to induce ovarian ODC activity increased markedly between anestrus and first proestrus, declining thereafter, and again paralleled the changes in LH receptor content. Evaluation of the kinetics of binding of hCG and FSH with their respective receptors in ovaries of 28-day-old rats revealed that the binding of hCG reached equilibrium within 4-8 h, whereas the binding of FSH attained equilibrium between 12-24 h. In both cases, however, the labeled hormones were clearly dissociable from their respective receptors by addition of an excess of unlabeled hormone. Moreover, although the ovarian receptor content of both hCG and FSH increased during prepubertal development, the equilibrium association constant of either hormone with its receptor remained unchanged. The results suggest that the infantile increase in FSH receptors may be induced by the high serum FSH levels present at that age and that, as shown by others in hypophysectomized rats, the subsequent increase in hCG receptors is, at least in part, an FSH-dependent phenomenon. The parallel changes in hCG receptors and LH-induced ODC activity during pre- and peripubertal development strongly suggest that an increase in LH binding capacity plays a fundamental role in the process of ovarian growth. It is also suggested that the changes in the steroidogenic ovarian response to hCG previously observed in peripubertal rats are, at least in part, determined by changes in ovarian LH receptor content.
Animals↗
Delayed puberty induced by chronic suppression of prolactin release in the female rat.
To study the effect of PRL deficiency on the onset of puberty, PRL release was chronically inhibited by treating immature female rats with the dopaminergic receptor agonist, bromoergocriptine (CB-154). The resulting alterations in the time of puberty onset, and in other associated parameters, such as serum levels of pituitary hormones, ovarian responsiveness to gonadotropins and ovarian hCG receptor content were then evaluated. CB-154 was provided in the drinking water from day 22 onward at the concentration of 20 and 100 micrograms/ml. The treatment resulted in almost complete suppression of serum PRL levels throughout the entire period studied (day 22 to first diestrus). In contrast, serum GH, FSH, and LH levels were not depressed. Likewise, pulsatile release of FSH was not affected and only a subtle alteration in pulsatile LH release was apparent. The onset of puberty, as determined by the age at vaginal opening, and at first diestrus after the first estrus and by the presence of corpora lutea at sacrifice (first diestrus), was markedly delayed in the hypoprolactinemic (HPO) rats. This inhibitory effect of CB-154 was completely prevented by concomitant administration of PRL. Ovarian weight was significantly decreased in HPO rats at the three ages studied (27, 32, and 36 days of age). By day 36, 50% of the control animals had already ovulated, as compared with only 9% of the HPO rats. Microscopic examination of ovaries from HPO rats revealed a retarded follicular development. In vitro ovarian progesterone response to hCG studied at day 32 and 36 of age was reduced in the HPO rats. Uterine growth was also depressed in HPO rats, the ovaries of which, when incubated in vitro, failed to show the prepubertal increase in estrogen response to hCG seen in control rats between day 32 ad 36. Aromatase activity, as measured by the in vitro release of estradiol from ovaries incubated in the presence of an excess of androgen substrate, was depressed in HPO rats. hCG receptor content in the ovaries from HPO rats (counts per min [125]hCG bound per micrograms DNA) was also lower than that of control animals at day 32 and 34 but not at day 36. However, at this later time the hCG receptor content per milligram of ovary was still significantly reduced in HPO rats. The results support the view that PRL plays an important role in the process of ovarian development that leads to the onset of puberty in the female rat and that this effect is, at least in part, exerted through a positive influence of PRL on ovarian LH receptor content.
Animals↗
Current studies on the mechanisms underlying the onset of female puberty.
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Adolescent↗
Recent advances in the endocrinology of puberty.
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Adolescent↗
Histological changes following the surgical closure of a canine cleft palate.
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Animals↗
Mechanisms involved in deglutition in Gallus domesticus.
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Animals↗
On vagal afferent control of avian breathing.
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Animals↗