Ovarian Gonadotropin Receptors Research Articles

Long-term role of neonatal microglia and monocytes in ovarian health.

Early life microglia are essential for brain development, and developmental disruption in microglial activity may have long-term implications for the neuroendocrine control of reproduction. We and others have previously shown that early life immune activation compromises the long-term potential for reproductive function in females. However, the supportive role of microglia in female reproductive development is still unknown. Here, we examined the long-term programming effects of transient neonatal microglial and monocyte ablation on hypothalamic-pituitary-gonadal (HPG) axis function in female rats. We employed a Cx3cr1-Dtr transgenic Wistar rat model to acutely ablate microglia and monocytes, commencing on either postnatal day (P) 7 or 14, since the development of the HPG axis in female rodents primarily occurs during the first two to three postnatal weeks. After an acutely diminished expression of microglia and monocyte genes in the brain and ovaries, respectively, microglia had repopulated the brain by P21, albeit that cellular complexity was still reduced in both groups at this time. Removal of microglia and monocytes on P7, but not P14 reduced circulating luteinising hormone levels in adulthood and ovarian gonadotropin receptors mRNA. These changes were notably associated with fewer primary and antral follicles in these rats. These data suggest that transient ablation of microglia and monocytes at the start of the second but not the third postnatal week has long-term effects on ovarian health. The findings highlight the important developmental role of a healthy immune system for female potential reproductive capacity and the importance of critical developmental periods to adult ovarian health.

Environmental impacts on the gonadotropic system in female Atlantic salmon (Salmo salar) during vitellogenesis: Photothermal effects on pituitary gonadotropins, ovarian gonadotropin receptor expression, plasma sex steroids and oocyte growth

The gonadotropic system and ovarian growth and development were studied during vitellogenesis in female Atlantic salmon subjected to either simulated natural photoperiod and ambient water temperature (NL-amb), or an accelerating photoperiod (short day of LD8:16 from May 10) combined with either warmed (ca 2°C above ambient; 8L-warm) or cooled water (ca 2°C below ambient; 8L-cold) from May to September.Monthly samples were collected from 10 females/group for determination of transcript levels of pituitary gonadotropin subunits (fshb and lhb) and ovarian gonadotropin receptors (fshr and lhr), plasma sex steroids (testosterone: T and estradiol-17β: E2), gonadosomatic index (GSI) and oocyte size.Short day in combination with either warmed or cooled water induced an earlier increase in pituitary fshb and lhb levels compared with NL-amb controls, and advanced ovarian growth and the seasonal profiles of T, E2. By contrast only minor effects were seen of the photothermal treatments on ovarian fshr and lhr.The 8L-cold had earlier increase in fshb, lhb and E2, but similar oocyte and gonadal growth as 8L-warm, suggesting that the 8L-cold group tried to compensate for the lower water temperature during the period of rapid gonadal growth by increasing fshb and E2 production.Both the 8L-warm and 8L-cold groups showed incomplete ovulation in a proportion of the females, possibly due to the photoperiod advancement resulting in earlier readiness of spawning occurring at a higher ambient temperature, or due to some reproductive dysfunction caused by photothermal interference with normal neuroendocrine regulation of oocyte development and maturation.

Pituitary gonadotropin and ovarian gonadotropin receptor transcript levels: Seasonal and photoperiod-induced changes in the reproductive physiology of female Atlantic salmon (Salmo salar)

In female Atlantic salmon kept at normal light conditions, pituitary follicle-stimulating hormone beta (fshb) transcript levels were transiently elevated one year before spawning, re-increased in February, and remained high during spawning in November and in post-ovulatory fish in December. The first increase in plasma 17b-estradiol (E2), testosterone (T) and gonadosomatic index (GSI) was recorded in January; E2 rose up to one month prior to ovulation, while T and GSI kept increasing until ovulation. Pituitary luteinizing hormone beta (lhb) transcript levels peaked at the time of ovulation. Except for transient changes before and after ovulation, ovarian follicle stimulating hormone receptor (fshr) transcript amounts were relatively stable at a high level. By contrast, luteinizing hormone receptor (lhcgr) transcript levels started out low and increased in parallel to GSI and plasma E2 levels. Exposure to continuous light (LL) induced a bimodal response where maturation was accelerated or arrested. The LL-arrested females showed previtellogenic oil droplet stage follicles or primary yolk follicles only, and fshb and E2 plasma levels collapsed while fshr increased. The LL-accelerated females showed elevated lhb transcript levels and slightly elevated E2 levels during early vitellogenesis, and significantly elevated lhcgr E2 and GSI levels in late vitellogenesis. We conclude that Fsh-dependent signaling stimulates recruitment into and the sustained development through vitellogenesis. Up-regulation of lhcgr gene expression during vitellogenesis may reflect an estrogenic effect, while elevated fshr gene expression following ovulation or during LL-induced arrestment may be associated with ovarian tissue remodeling processes.

The ovarian gonadotropin receptors in health and disease.

The ovarian gonadotropin receptors in health and disease.

Gonadotropins and ovarian gonadotropin receptors during the perimenopausal transition period

Gonadotropins and ovarian gonadotropin receptors during the perimenopausal transition period

Gonadotropins and ovarian gonadotropin receptors during the perimenopausal transition period

As an early sign of perimenopause, the menstrual cycles become irregular. Associated with this irregularity, serum gonadotropin levels increase. There are studies correlating these changes to ovarian follicular morphology and number, but no reports are available, to our knowledge, correlating the increases in gonadotropin levels to respective cellular receptors. In fact, the regulation of gonadotropin receptors is poorly understood in the human. The action of gonadotropins on gonadal function is mediated through specific binding of the hormones to receptors located on the surface of target cells followed by activation of intracellular second messenger systems. In the ovary, the target cells for FSH are granulose cells of ovarian follicles, while the action of LH is mediated through binding of the ligand to theca, granulosa and luteal cells. The cell-surface receptors for gonadotropins are located respectively on these cell types. The molecular nature of FSH receptors and LH receptors has been characterized in many species, and their structure is well-known both on the protein and nucleic acid level. Despite the vast amount of studies in rodents, there is limited information available on the regulation of gonadotropin receptors in the human. In a recent study, serum LH and FSH levels were correlated to respective receptor levels in ovarian tissue in order to better understand gonadotropin action and the physiology of the menopause in the human. High serum gonadotropin levels in perimenopause suggested the existence of low ovarian gonadotropin receptor levels. In most patients who are still experiencing cyclic menstrual bleeding no FSH receptors were detected possibly due to severe disturbances in follicular FSH receptor synthesis prior to ovarian follicle exhaustion.

Gonadotropins and gonadotropin receptors during the perimenopause.

Twenty-two perimenopausal patients (aged 47-56 years) admitted for elective abdominal hysterectomy and salpingo-oophorectomy were selected to understand better the clinical significance of increasing gonadotropin levels as an indicator of target organ responsiveness. Prior to anesthesia, blood was drawn from the patients for subsequent analyses of serum follicle-stimulating hormone (FSH), luteinizing hormone (LH) and 17beta-estradiol (E2) levels. Ovarian tissue was obtained during surgery and frozen at -70 degrees C for subsequent analyses for FSH and LH receptor content. The phase of the menstrual cycle of the patients or postmenopause was determined by serum gonadotropin and E2 levels and histological evaluation of the endometrium. Patients with no detectable FSH receptors showed significantly higher serum FSH and LH levels (4.7- and 4.3-fold, respectively) when compared to patients with detectable FSH receptors; FSH receptors were present in 27% of the patients, LH receptors were present in 68% of the patients and a negative correlation was found between serum LH levels and ovarian LH receptors. In postmenopausal patients, neither FSH receptors nor LH receptors were detectable. High serum gonadotropin levels in perimenopausal patients thus suggest the existence of low or undetectable ovarian gonadotropin receptor levels.

Effect of 80 kDa protein of porcine follicular fluid on gonadotropin stimulated progesterone production in rat granulosa cells in vitro

We reported the presence of a 80 kDa polypeptide in porcine follicular fluid that inhibited the binding of 125I-radiolabelled hFSH as well as hCG to the rat ovarian gonadotropin receptors. In the present study, the biological activity of the receptor binding inhibitor is determined using an in vitro bioassay procedure. Granulosa cells isolated from PMSG primed immature rat ovaries respond to exogenously added gonadotropins in terms of progesterone production. Addition of fractions containing the gonadotropin receptor binding inhibitory activity inhibited progesterone production stimulated by the gonadotropins in a dose-dependent fashion. The receptor binding inhibitory activity was also capable of inhibiting progesterone production stimulated by PMSG, which has both FSH- and LH-like activities in rats. In contrast, progesterone production stimulated by dbcAMP was not inhibited by the receptor binding inhibitor. This result indicates that the site of action of the inhibitor is proximal to the formation of the cAMP. The above observations point out to a possible role for this factor in modulating gonadotropin activity at the ovarian level.

Characterization of ovarian gonadotropin receptor. Monomer and associated form of the receptor.

We have purified luteinizing hormone/human choriogonadotropin (hCG) receptor from rat ovary by sequential affinity column on wheat germ lectin-Sepharose and hCG-Sepharose chromatography. The purified receptor, previously identified as a single protein on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) (Kusuda, S., and Dufau, M.L. (1986) J. Biol. Chem. 261, 16161-16168), was further characterized by radioiodination with 1,3,4,6-tetrachloro-3 alpha, 6 alpha-diphenylglycouril, and column chromatography on wheat germ lectin-Sepharose. Autoradiography of SDS-PAGE analysis under reducing conditions showed a single radiolabeled band of Mr = 80,000. The radioiodinated receptors treated with peptide:N-glycosidase F migrated at Mr = 54,000. Treatment with neuraminidase alone caused only a minor reduction in molecular weight, and subsequent treatment with endo-alpha-N-acetyl-D-galactosaminidase had little further effect on the receptor. When the radioiodinated receptor was analyzed by fast protein liquid chromatography, a single broad peak was eluted with Mr of approximately 350,000. The higher Mr of radioiodinated receptors than that of native receptors (Mr = 190,000 dimeric form) could be due to the aggregation of labeled molecules. These complexes dissociated into the monomeric form in the presence of SDS. To determine whether the monomers can bind hormone, the purified unlabeled receptors resolved with SDS were electroblotted to nitrocellulose membranes and incubated with 125I-hCG. Autoradiograms of the blots showed a band of monomer (Mr = 78,000) as well as one of dimer (Mr approximately 150,000). These studies have demonstrated that the luteinizing hormone/hCG receptors are predominantly N-linked glycosylated and suggest that the native receptor is a dimer of identical hormone binding subunits associated by noncovalent interactions. Although the individual subunits can bind hormone, it is conceivable that the dimeric form is necessary for signal transduction.

Enhanced ovarian gonadotropin receptors in the testosterone-induced polycystic ovary in rats.

To establish the role of hormone receptors in patients with polycystic ovary (PCO), PCO rats were prepared by treating with testosterone propionate (TP). Five-day old immature female rats were subcutaneously injected with 1.25 mg TP in sesame oil. They were then killed at the age of 12 weeks. The ovarian receptors for LH and FSH as well as serum hormone levels were investigated in PCO rats and also in control rats at the various stages of the estrous cycle. The LH receptor binding in the TP-treated ovaries was elevated almost as high as that of proestrus control, and was observed to be higher than the other control. The FSH receptor binding of PCO rats was elevated to 173% of that of diestrus control, which showed the highest value throughout the cycle. Thus, the gonadotropin receptors in PCO rats appeared to be in an activated state. High levels of the receptor binding were due to an increase in receptor binding sites. Serum LH level was significantly higher than that of diestrus control but still remained lower than that of proestrus control. In contrast, FSH level was as low as that of diestrus control. Prolactin level was markedly elevated and 17- and 2-fold higher than that of diestrus and proestrus control, respectively. Estradiol level was higher than that of diestrus control, increasing to almost the same level during proestrus control. While progesterone level was largely depressed to 23 and 13% of that of diestrus and proestrus control, respectively, testosterone level was almost the same as that of diestrus control. From these results, it was suggested that tonic secretion of LH, low level of FSH, and markedly high levels of prolactin would increase the gonadotropin receptors and result in extremely low production of progesterone in rat ovaries. Clinically, elevated levels of the LH and FSH receptors may be a relevant occurrence in PCO patients.

Ovarian gonadotropin receptors during experimental ovarian cyst formation in the rat.

Polycystic ovaries, produced in hypothyroid rats by 20 daily injections of hCG, were examined during developmental stages for their content of LU and FSH receptors by means of the specific binding of 125 l-hCG and ‘�‘ I-FSH to ovarian homogenates. Scatchard plot analysis indicated that the decline in FSH receptor population that occurred in control animals during the 30 day experimental period was significantly retarded by feeding thiouracil, whereas receptors for hCG (LH) were unaffected, Within I day of beginning hCG injections on Day 11, ovarian receptors to both FSH and hCG declined precipitously in all animals. The loss in FSH receptors, however, was retarded by thiouracil so that ovarian FSH receptor content remained more than twice that of euthyroid animals during the first 5 days of ovarian cyst induction, This difference disappeared by the end of 20 days of injections by which time extensive ovarian cyst formation had taken place in the hypothyroid animals. The present work indicates that an enhanced ovarian binding of FSH in hypothyroid animals at the onset of hCG activation of the tissue could explain the excessive follicular response, without ovulation or atresia, which leads to continued growth and fluid accumulation of the cysts.

Relative importance of the adenohypophyseal and gonadal sites in inhibitory action of LHRH agonists.

Assessment of the role of endogenous LH release and direct gonadal action of LHRH agonists in the loss of gonadal LH receptors induced by treatment with gonadotropin-releasing peptides was first made by comparing the effect of single administration of 1 �g of ID-Ala’, des-Gly-NH2 ‘#{176} I LHRH ethylamide, ED-Ala’) LHRH-EA, 12 h before or immediately after hypophysectomy (HYPOX) on LH receptor levels measured 48 h after surgery in male and female adult rats. While administration of the LHRH agonist before HYPOX leads to a 50% loss of testicular LH receptors, only a 20% decrease is seen in HYPOX animals, thus suggesting a predominant role of endogenous LH release in the desensitization process in male animals. Treatment with increasing doses (1 to 100 ng/day) of another LHRH agonist, [D-Ser(TBU)’ I LHRH-EA, causes a 90% loss of testicular LH receptors in intact rats at the highest dose used (100 ng daily for 9 days) while the same treatment decreases LH receptors by only 35% in HYPOX animals. As measured by the steroidogenic response to 10 �g 0LH in vivo, while treatment of intact animals with [D-Ser(TBU)’ I LHRHEA leads to a marked blockage of the testicular steroidogenic pathway at the level of 17-hydroxylase and 17,20-desmolase activities with a corresponding increase of 5o-reductase activity, minimal or no signs of changes of enzymatic activity are seen after identical treatment in HYPOX animals. Chronic treatment (1 month) with the LHRH agonist in intact rats leads to degenerative changes of the seminiferous tubules, while no effect is observed in HYPOX animals, thus suggesting the essential role of the pituitary gland. Moreover, adrenalectomy does not influence the inhibitory effect of treatment with LHRH agonists on the loss of testicular LH receptors in HYPOX animals, thus eliminating the role of the adrenals in the action of LHRH agonists. Contrary to the results obtained in male animals, single administration of the LHRH agonist in female rats has similar inhibitory effects on ovarian gonadotropin receptors when administered either before or after hypophysectomy. Moreover, treatment with increasing doses of ED-Ser(TBU)’ I LHRH-EA leads to a similar inhibition of ovarian LH receptor levels in intact and HYPOX female animals. The present data show that LHRI-I agonist-induced endogenous LH release plays a predominant role in the desensitizing effect of treatment with LHRH agonists on testicular LH receptors and steroidogenesis as well as on inhibition of spermatogenesis; in the female, the direct gonadal effect, at least on LH and FSH receptors, appears to play a more important role than in male animals.

Regulation of ovarian gonadotropin receptors and LH bioactivity during the estrous cycle

FEBS LettersVolume 122, Issue 2 p. 184-188 Full-length articleFree Access Regulation of ovarian gonadotropin receptors and LH bioactivity during the estrous cycle A.R. Solano, A.R. Solano Molecular Endocrinology Section, Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20205, USASearch for more papers by this authorA.Garcia Vela, A.Garcia Vela Molecular Endocrinology Section, Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20205, USASearch for more papers by this authorK.J. Catt, K.J. Catt Molecular Endocrinology Section, Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20205, USASearch for more papers by this authorM.L. Dufau, Corresponding Author M.L. Dufau Molecular Endocrinology Section, Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20205, USAAddress correspondence and reprint requests to M. L. D.: National Institutes of Health, Bldg. 10, 12N-216, Bethesda, MD 20205, USASearch for more papers by this author A.R. Solano, A.R. Solano Molecular Endocrinology Section, Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20205, USASearch for more papers by this authorA.Garcia Vela, A.Garcia Vela Molecular Endocrinology Section, Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20205, USASearch for more papers by this authorK.J. Catt, K.J. Catt Molecular Endocrinology Section, Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20205, USASearch for more papers by this authorM.L. Dufau, Corresponding Author M.L. Dufau Molecular Endocrinology Section, Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20205, USAAddress correspondence and reprint requests to M. L. D.: National Institutes of Health, Bldg. 10, 12N-216, Bethesda, MD 20205, USASearch for more papers by this author First published: December 29, 1980 https://doi.org/10.1016/0014-5793(80)80433-9Citations: 9AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat References 1 A.J.-W. Hsueh, M.L. Dufau, K.J. Catt, Proc. Natl. Acad. Sci. USA, 74, (1977), 592– 595. 2 R.M. Sharpe, Biochem. Biophys. Res. Commun., 76, (1977), 957– 962. 3 K.W. Cheng, J. Reprod. Fert., 48, (1976), 129– 135. 4 M.L. Dufau, G.D. Hodgen, A.L. Goodman, K.J. Catt, Endocrinology, 100, (1977), 1557– 1560. 5 A.R. Solano, M.L. Dufau, K.J. Catt, Endocrinology, 105, (1979), 372– 381. 6 K.J. Catt, A.J. Baukal, T.F. Davis, M.L. Dufau, Endocrinology, 104, (1979), 17– 25. 7 M.L. Dufau, E. Beitins, J. McArthur, K.J. Catt, P. Troen H.R. Nankin The Testis in Normal and Infertile Men (1977), Raven New York 309– 326. 8 R.L. Butcher, W.E. Collins, N.W. Fugo, Endocrinology, 94, (1974), 1704– 1708. 9 J.D. Neill, M.S. Smith, V.H.T. James L. Martini Current Topics in Experimental Endocrinology 2, (1974), Academic Press New York 73– 106. 10 M. Conti, J.P. Harwood, M.L. Dufau, K.J. Catt, Mol. Pharmacol., 13, (1977), 1024– 1032. 11 A. Nimrod, E. Bedrak, S.A. Lamprecht, Biochem. Biophys. Res. Commun., 78, (1977), 977– 984. 12 B.I. Posner, P.A. Kelly, H.G. Friesen, Science, 188, (1975), 57– 59. 13 H.R. Behrman, D.T. Armstrong, Endocrinology, 85, (1969), 474– 478. 14 A. Garcia-Vela, A.R. Solano, Endocrinology, 106A, (1980), 621– Citing Literature Volume122, Issue2December 29, 1980Pages 184-188 ReferencesRelatedInformation

Inhibitory Effects of Long Term Treatment with a Luteinizing Hormone-Releasing Hormone Agonist on the Pituitary-Gonadal Axis in Male and Female Rats

Following previous observations of the potent antifertility effects of acute treatment with LHRH or its agonistic analogs in male and female rats, this study describes the effect of long term (up to 12 weeks) treatment with an LHRH agonist, [D-Ala6, des-Gly-NH210]LHRH ethylamide (LHRH-A), on testicular and ovarian gonadotropin receptor levels and function in the rat. Treatment of adult male rats with 100 ng LHRH-A every third day led to a progressive decrease of testis, seminal vesicle, and prostate weight up to 12 weeks of treatment, while the inhibitory effect (70%) on LH receptor levels was already maximal at 1 week. When adult female rats were injected daily with 5 microgram LHRH-A for 12 weeks, ovarian LH, FSH, and PRL receptor levels were reduced 50--90%, while plasma estradiol and progesterone levels were inhibited 60% (compared with diestrus day 1). The effect of chronic administration of a low dose (5 IU) of hCG in the male rat was transient. By contrast, no sign of resistance developed up to 12 weeks of treatment with the LHRH agonist in either male or female animals.

Inhibition of Ovarian Luteinizing Hormone (LH) and Follicle-Stimulating Hormone Receptor Levels With an LH-Releasing Hormone Agonist During the Estrous Cycle in the Rat

A single injection of the luteinizing hormone (LH)-releasing hormone (LHRH) agonist [D-Ala6,des-Gly-NH2(10)]LHRH ethylamide to female rats on diestrus I produced a marked reduction in ovarian LH/human chorionic gonadotropin (hCG) and follicle-stimulating hormone (FSH) receptor levels, uterine weight, and plasma progesterone levels measured 2 days later on expected proestrus. A maximal inhibitory effect was seen after a dose of only 40 ng of the peptide. No consistent effect of the LHRH analog was seen on ovarian prolactin receptors. When the analog was injected on day 7 of pregnancy, the inhibition of ovarian LH/hCG receptors was of shorter duration and was much less sensitive than that in nonpregnant animals. These data indicate that ovarian LH and FSH receptors levels are highly sensitive to changes in endogenous gonadotropin secretion and suggest that the gonadotropin surge occurring spontaneously on proestrus may play an important role in the regulation of ovarian gonadotropin receptors during the estrous cycle.

Inhibitory Effect of a Luteinizing Hormone (LH)-Releasing Hormone Agonist on Rat Ovarian LH and Follicle-Stimulating Hormone Receptor Levels During Pregnancy

When injected at the daily dose of 100 microgram on days 7 through 12 of pregnancy, the luteinizing hormone (LH)-releasing hormone (LHRH) agonist [D-Ala6, des-Gly-NH2(10)] LHRH ethylamide led to complete suppression of pregnancy and a 45% to 60% decrease in plasma progesterone concentration. The antifertility effect of the LHRH analog was accompanied by an early and almost complete inhibition of ovarian LH/human chorionic gonadotropin and follicle-stimulating hormone receptor levels. These data suggest that the antifertility effects of LHRH agonists are mediated by down-regulation of ovarian gonadotropin receptors and decreased luteal function.

Physical characteristics of the gonadotropin receptor-hormone complexes formed in vivo and in vitro.

The physical properties of detergent-solubilized gonadotropin receptor-hormone complexes, determined by density gradient centrifugation and gel filtration, were compared after in vivo and in vitro labeling of specific ovarian binding sites with radioiodinated human chorionic gonadotropin (hCG). Following intravenous administration of biologically active 125I-labeled hCG, up to 50% of the gonadotropin tracer was bound to the luteinized ovaries of immature female rats treated with pregnant mare serum/human chorionic gonadotropin. Comparable binding of 125I-labeled hCG was observed after equilibration of ovarian particles with the labeled hormone in vitro. The sedimentation properties of the solubilized receptor-hormone complexes formed in vivo were identical with those derived for the corresponding complexes formed in vitro and extracted with Triton X-100 and Lubrol PX, with sedimentation constants of 8.8 S for the Triton-solubilized complex and 7.0 S for the complex extracted with Lubrol PX. During analytical gel filtration of the Triton-solubilized receptor-hormone complex on Sepharose 6B in 0.1% Triton X-100, the partition coefficient (Kav) of the "in vivo" complex (0.32) was not significantly different from that of the complex formed in vitro (0.29). Gel filtration of the Lubrol-solubilized ovarian particles on Sepharose 6B in 0.5% Lubrol PX gave Kav values for the "in vivo" and "in vitro" labeled complexes of 0.36 and 0.32, respectively. These findings demonstrate that the physical properties of size and shape which determine the partition coefficient and sedimentation characteristics of detergent-solubilized gonadotropin receptor-hormone complexes formed in vitro are not distinguishable from those of the complexes extracted after specific interaction of the ovarian gonadotropin receptors with radioiodinated hCG in vivo.