Exogenous Gonadal Steroids Research Articles

Hormonal contraception is not associated with increased risk for seizures in the general population: results from a cohort study using The Health Improvement Network.

Endogenous human gonadal steroids and especially female sex hormones modulate the risk of developing epileptic seizures. In most circumstances, estrogens increase excitability, while progesterone bears substantial anticonvulsive properties. We questioned whether exogenous gonadal steroids used as hormonal contraception are associated with risk of seizures. In a dynamic cohort ascertained within The Health Improvement Network database, we identified 2201 female patients aged 20-44years with seizures during follow-up. In a nested case-control analysis, we matched these cases to 10,143 controls. Using logistic regression, we calculated the risk of seizure associated with use of contraceptives and adjusted for potential confounders. We performed same analyses among women with no prior hormonal contraception use ("new user" analyses) and in patients with a history of epilepsy. Unadjusted data suggested a lower risk for seizures in patients taking exogenous gonadal steroids irrespective of type of contraception used. After adjustment for potential confounders, neither use of combined oral contraceptives nor progestin-only oral contraceptives was associated with the risk for seizures overall. Analyses of "new users" of oral contraceptives produced similar risk estimates. We found no evidence supporting an effect of oral exogenous gonadal steroids used for hormonal contraception on the risk of seizures in the general female population.

A Pilot Study of Muscle‐Nerve‐Muscle Grafting for Facial Reanimation in Rats

Objectives: (1) Describe the muscle-nerve-muscle (MNM) reinnervation technique, which involves implanting a graft to serve as a conduit between an innervated donor muscle and a denervated recipient muscle. (2) Analyze the effects of MNM reinnervation with and without electrical stimulation and exogenous testosterone on functional recovery following rat facial nerve injury. Methods: A prospective controlled animal study. Facial nerve branches to the whisker pads of 24 adult male Sprague Dawley rats were harvested and each rat was then randomly assigned to 1 of 3 treatment groups of 8 rats each: no graft (control), MNM grafting alone (MNM), or MNM grafting + electrical stimulation (ES) and testosterone propionate (TP) (MNM+). MNM grafts were implanted from the functioning to the nonfunctioning whisker pads in the experimental groups. One experimental group underwent an ES and TP protocol. Whisker movement was assessed by behavioral observations, electromyographic recordings, and video analysis. Results: Recovery of coordinated movement was displayed at 16 weeks by 0% of the control animals, 71% of the MNM animals, and 85% of the MNM+ animals. Electromyographic recordings demonstrated electrical conductance across grafts in both MNM and MNM+ animals. Histologic analysis of the MNM grafts demonstrated growth of myelinated fibers across nerve grafts in both MNM and MNM+ animals. Conclusions: This study demonstrated not only that reinnervation following MNM grafting can improve tone and movement in a selected muscle following a facial nerve injury, but also that therapy with electrical stimulation and exogenous gonadal steroids further enhances the recovery of these functional measures.

Effect of Exogenous Gonadal Steroids on Reproductive Functions of the Indian Pygmy Field Mouse Mus terricolor

Different thresholds of gonadal steroids exert stimulatory or inhibitory effects on GnRH and gonadotropin release. During the reproductively active phase (RAP), the concentration of endogenous gonadal steroids remains high while, during reproductively inactive phase (RIP), it remains low. During RIP the HPG axis is sensitive to gonadal steroids but the circulatory levels of testosterone and estradiol remain low. During this phase one can observe conveniently the effects of gonadal steroids on the HPG axis in male or female rodents. Therefore, the aim of the present study was to find the effects of testosterone and estradiol on the reproductive functions of male and female Indian pygmy field mouse, Mus terricolor , during RIP. The male mice were injected aquaviron (commercially available testosterone, 1mg/100g body weight) while the female mice received estradiol-benzoate (25μg/100g body weight) for 15 consecutive days during the RIP. After completion of the treatment, a significant increase in the weights of gonads and accessory sex organs was noted in both the sexes. The biochemical constituents of accessory sex organs such as epididymal sialic acid, seminal vesicular fructose and uterine protein content reflected significant elevation accompanied by increased levels of plasma testosterone, estradiol and progesterone. Histologically, the gonads and accessory sex organs exhibited increased cellular activity. However, the gonadal cholesterol was significantly decreased in both the sexes. Over all, administration of gonadal steroids to both male and female mice accelerated the gonadal recrudescence but did not inhibit the reproductive functions when administered during the RIP. Therefore, it can be inferred from the present study that during the RIP the HPG axis is sensitive to gonadal steroids and, hence, exogenous gonadal steroids induce gonadal activity.

Effects of exogenous melatonin on Bax and P53 expression in substantia nigra of adult rat menopause model following pinealectomy

Background: Melatonin which also called “dark hormone” is released from the pineal gland and is well known for its role in regulating biological rhythms in all mammals. Recently more other functions have been reported for melatonin. Among these roles, its function as an antioxidant is more emphasized by researchers. Recent findings also have showed reciprocal interaction between gonadal hormones and nervous system. Gonadal hormones have dramatic genomic and non-genomic effects on certain structures of the brain. Substantia nigra (SN) which is the main source of dopaminergic outputs is influenced by female sex hormones; it has also intercellular receptors for melatonin. In order to find the co-effects of exogenous melatonin and gonadal steroid deprivation on SN the present research was done. Material and methods: Fifty adult female Sprague-Dawley rats were used in this study. The animals randomizely divided into groups including pinealectomized (PX), ovariectomized (OVX) with and without exogenous melatonin, PX+ OVX with and without exogenous melatonin, sham and control groups were also considered. Pinealectomy was done after 4 weeks of ovariectomy. Three weeks after pinealectomy the animals received 20 mg/kg melatonin for 60 days. On day 60 the animals perfused and fixed, their brain removed and prepared for TUNEL staining. By using western blotting, Bax and P53 protein expression in SN was assayed. Results: Our findings with TUNEL staining showed the number of apoptotic nuclei of the animals which treated by injection of melatonin 20 mg/kg after 10 days was significantly less than the PX, OVX and PX+OVX groups (p< 0.001). The western blotting analysis showed that the expression of Bax proapoptotic protein in OVX + mel, PX+ mel and OVX+PX+ mel showed significant decrease compared with PX, OVX and PX+OVX groups. We found the same results for expression of P53. Conclusion: Based on our findings the role of melatonin as an antioxidant to prevent cell loss was confirmed. In addition; it seems that there is no dominancy in cell death preventing between exogenous melatonin and female gonadal steroids.

Use of Growth Hormone Secretagogues to Prevent or Treat the Effects of Aging: Not Yet Ready for Prime Time

In this issue, Nass and colleagues report that at 1 year, an oral ghrelin mimetic increased pulsatile growth hormone secretion and morning insulin-like growth factor I concentration to that in heal...

Cortisol and memory retrieval in women: influence of menstrual cycle and oral contraceptives

Studies in rodents observed that the effects of stress on memory are modulated by gonadal hormones. In animals and humans, stress and cortisol treatment impairs memory retrieval. To investigate if the acute impairing effect of cortisol on memory retrieval in women is influenced by endogenous or exogenous gonadal steroids. Three groups of women were studied: women during mensis (n=13), women in the luteal phase (n=14), and women using oral contraceptives (OCs; n=20). In a double-blind crossover fashion, they received cortisol (30 mg) or placebo 1 h prior to memory retrieval testing. Overall cortisol led to a significant impairment of memory retrieval. Further exploratory analysis using t tests showed that both groups of naturally cycling women were significantly impaired (p<0.05), while no effect was apparent in the OC users (p=0.29). The current results could suggest that OC use is associated with a reduced sensitivity of the brain to acute cortisol elevations. In contrast, menstrual-cycle-associated changes in estradiol and progesterone concentrations appear to have no strong influence on this acute cortisol effect. The underlying neurobiological mechanisms of these behavioral findings remain to be elucidated.

Sex hormones, insulin sensitivity, and diabetes mellitus.

Sex differences and the role of gonadal hormones in modulating insulin sensitivity and glucose tolerance are of increasing interest and importance because of the increasing prevalence of type 2 diabetes mellitus and the metabolic abnormalities associated with aging. Body composition is closely associated with insulin sensitivity, and increased body fat, particularly in the visceral compartment, is a risk factor for developing type 2 diabetes mellitus. Sex differences in body composition and/or insulin sensitivity are evident in humans throughout the lifespan. Ovarian hormones influence insulin sensitivity across the menstrual cycle, during pregnancy, and in the menopausal transition. Similarly, estrogens and progestins used for contraception and hormone replacement therapy affect glucoregulation. Nonhuman primates and humans have similar life histories and reproductive characteristics. As a result, nonhuman primates provide a valuable model for investigating factors related to insulin sensitivity. Studies of nonhuman primates have contributed significantly to our understanding of sex differences and the influence of sex steroids in this context. This brief review surveys present knowledge of the sex differences in body composition, insulin sensitivity, and risk for development of type 2 diabetes mellitus derived from studies in humans and nonhuman primates. The influences of endogenous and exogenous gonadal steroids are emphasized.

Adaptive interactions between cytokines and the hypothalamic-pituitary-gonadal axis.

Circulating and tissue concentrations of pyrogenic cytokines, especially interleukin (IL)-1 beta, vary temporally through the menstrual cycle and pregnancy. The secretion of these cytokines in vitro by isolated human mononuclear cells is significantly influenced by exogenous gonadal steroids and gonadotropins. Reciprocally, cytokines influence gonadotropin secretion by the pituitary and steroidogenesis by the ovaries and testes. Several hypotheses have been advanced regarding the adaptive value of these interrelationships. Cytokine-induced synthesis of proteolytic enzymes and extracellular matrix proteins may be important for the tissue remodeling necessary for ovulation, implantation, and delivery. Tolerance of the fetal allograft may require downregulation of cytotoxic effector cells and reciprocal upregulation of humoral and nonspecific host defenses. The inhibitory influence of IL-1 beta on the luteinizing hormone surge may prevent inopportune conception, and the abortive influences of tumor necrosis factor-alpha and gamma interferon may terminate pregnancy during periods of infection.

A revised critical period for the sexual differentiation of the sexually dimorphic nucleus of the preoptic area in the rat.

The volume of the sexually dimorphic nucleus of the preoptic area (SDN-POA) of the rat is several times larger in males than in females. Several studies have established the importance of gonadal steroids perinatally in the sexual differentiation of the SDN-POA as well as a critical period for the permanent influences of exogenous androgen on the volume of the nucleus. Recent preliminary evidence from this laboratory had suggested, however, that the critical period for the effects of the removal of endogenous gonadal steroids on SDN-POA volume may not match that for the administration of exogenous gonadal steroids. A series of experiments was designed to examine further the effects of the removal of endogenous gonadal steroids on adult SDN-POA volume by castrating male rats at various ages. In spite of a rather clear definition of a postnatal critical period for the effects of exogenous steroid administration, the results of this study indicate that the volume of the SDN-POA is sensitive to the removal of endogenous gonadal steroids for a prolonged period of time, extending through at least day 29 postnatally. The data suggest that there may be multiple critical periods for the sexual differentiation of the SDN-POA and reinforce the concept that these critical periods are distinct from those for other sexually differentiated parameters.

Gonadal steroid control of preprocholecystokinin mRNA expression in the limbic‐hypothalamic circuit: Comparison of adult with neonatal steroid treatments

The neuropeptide cholecystokinin (CCK) is involved in the regulation of female, but not male, reproductive behavior. In both sexes, estrogen regulates the expression of CCK in adulthood within the bed nucleus of the stria terminalis and medial amygdaloid nucleus. These areas are parts of an interconnected limbic system-hypothalamic circuit, the development of which is influenced by estrogen during the early postnatal period. This is the same period during which central nervous system (CNS) expression of CCK is dramatically increased, suggesting that the male and female patterns of CCK expression may be the result of early postnatal exposure to estrogen. In the present experiment, the expression of preprocholecystokinin (pCCK) mRNA was determined by in situ hybridization with an isotopically labeled pCCK complementary RNA and emulsion autoradiography in animals whose neonatal and adult gonadal steroid levels had been manipulated. The number of pCCK-expressing cells in animals that were gonadectomized as adults was determined by neonatal estrogen, but stimulation with steroids in adulthood induced a similar number of pCCK-expressing cells in both sexes in the medial amygdala and bed nucleus of the stria terminalis. Neonatal treatment of females with estrogen or testosterone, followed by ovariectomy in adulthood, eliminated the sex difference in pCCK mRNA expression. Males treated neonatally with the aromatase inhibitor androstenedione (to block metabolism of testosterone to estrogen) and orchidectomized in adulthood had a level of pCCK mRNA expression that was similar to that of ovariectomized females. These data suggest that, during neonatal development, estrogen determines the constitutive expression of pCCK mRNA in the medial amygdala and bed nucleus of the stria terminalis, resulting in higher levels of pCCK mRNA expression in males than in females. However, exogenous gonadal steroids induce the same levels of pCCK mRNA expression in adult females, indicating that the levels of gonadal steroids and the patterns of their secretion are the predominant influences on the sexually dimorphic adult levels of pCCK mRNA expression.

Influence of photoperiod and gonadal steroids on hibernation in the European hamster.

Torpor was monitored daily in adult male and female European hamsters (Cricetus cricetus) induced to hibernate by exposure to a cold environment (6 degrees C). The effect of photoperiodic manipulations or administration of exogenous gonadal steroids was examined in gonadectomized or intact hamsters. 1. Gonadal regression occurred in all short day, but only in some long day, cold-exposed hamsters. Entry into hibernation was not observed until reproductive regression had occurred. Thus, gonadal atrophy appears to be a necessary precondition for hibernation. 2. Castrated hamsters in the short day cold condition showed a significantly greater incidence of torpor than those in the long day cold condition. Hence, photoperiod affected torpor independently of its effect on the gonadal cycle. 3. Testosterone, when administered via silastic capsules at near physiological levels, completely inhibited torpor in gonadectomized male and female hamsters hibernating in the short day cold condition. 4. In ovariectomized females, torpor was unaffected by progesterone treatment, but partially inhibited by estradiol. A greater inhibition of torpor was observed when estradiol-primed females were administered both estradiol and progesterone simultaneously. Thus, the effect of both hormones may be functionally comparable to that of the single testicular hormone. 5. Estradiol inhibited torpor to a greater extent in intact and ovariectomized female hamsters hibernating in long days than those in short days, suggesting an effect of photoperiod on responsiveness to estradiol. These results indicate an inverse relationship between the gonadal and hibernation cycles, and a probable role for gonadal steroids to influence the timing of the hibernation season. However, non-gonadal factors must also be involved in controlling hibernation, since photoperiod affected the incidence of torpor in gonadectomized animals and because hamsters were able to terminate hibernation in the absence of gonadal hormones.

Neonatal exposure to DES in BALB/c male mice: Effects on pituitary-gonadal function

Neonatal male BALB/c mice were injected with diethylstilbestrol (DES), estradiol benzoate (E 2B), testosterone propionate (TP), progesterone or DES, in combination with E 2B, TP or progesterone and examined in adulthood. Body weight was reduced in males exposed to DES, TP or DES + TP, while testicular weight was reduced in animals injected with DES, E 2B, TP, DES + TP or DES + progesterone. Exposure to DES and/or E 2B also produced reproductive tract abnormalities and concomitant progesterone exposure did not further affect this parameter. Concomitant DES did not further alter the reduced plasma luteinizing hormone (LH) levels attributable to neonatal TP or E 2B treatment. Plasma follicle-stimulating hormone (FSH) levels in intact males were increased by DES, DES + progesterone or progesterone alone. Assessment of the feedback effects of exogenous gonadal steroids on pituitary gonadotropin release in castrated adults indicated that injection of 125 μg TP further increased the already elevated post-castration levels of LH and FSH in mice neonatally exposed to progesterone. The increase in testosterone (T) concentration after intratesticular human chorionic gonadotropin (hCG) administration was significantly attenuated in mice neonatally exposed to DES plus E 2B or to progesterone. Basal testicular T levels were significantly elevated in males exposed to DES, alone, or in combination with progesterone. Exposure to DES and TP increased hypothalamic serotonin (5-HT) levels in intact mice, while levels of 5-HT were lower after castration compared to controls. DES + E 2B-treated mice had higher norepinephrine (NE) levels, and E 2B-treated mice also had higher 5-HT levels. These findings indicate that alterations produced as a consequence of neonatal DES exposure include disruptions in pituitary-gonadal feedback and in brain biogenic amine levels, in addition to gross morphological abnormalities in the reproductive tract. Some of the effects of neonatal DES exposure were attenuated by simultaneous treatment with TP, E 2B or progesterone. In addition, treatment with these steroids was also capable of altering pituitary-gonadal feedback. However, gross genital abnormalities were apparent only in males receiving estrogenic preparations. Concomitant exposure to progesterone appeared to be capable of blocking DES-induced morphological effects.

Effect of exogenous gonadal steroids and pregnancy on uterine luminal prostaglandin F in mares

Two experiments were conducted to assess the effect of exogenous hormone treatment on uterine luminal prostaglandin F (PGF). In the first experiment ovariectomized pony mares received either corn oil (21 days, n = 3), estradiol valerate (21 days, n = 3), progesterone (21 days, n = 3) or estradiol valerate (7 days) followed by progesterone (14 days, n = 4). Progesterone treated mares had higher (P<.01) uterine luminal PGF compared with all other groups, and no differences were detected between other treatment comparisons. In Experiment II, uterine fluid was collected from 4 ovariectomized horse mares before and after treatment with estradiol valerate (7 days) followed by progesterone (50 days). Pretreatment uterine luminal PGF levels were lower (P<.001) than post-treatment levels (.03 vs 76.80 ng/ml). In a third experiment PGF was measured in uterine fluid of pony mares on days 8, 12, 14, 16, 18 and 20 of the estrous cycle and pregnancy. In nonpregnant mares a day effect P<.03) was observed in which uterine fluid PGF increased during the late luteal phase and declined thereafter. In contrast, no day effect was observed in pregnant animals and uterine luminal PGF was lower (P<.001) than in cycling animals. These studies indicate that exogenous progesterone administration results in a large increase in uterine luminal PGF, whereas, pregnancy results in suppression. Taken collectively with previous work from our laboratory, these results suggest that while the endometrium of pregnant mares is capable of producing large amounts of PGF, the presence of a conceptus impedes its synthesis and/or release which allows for luteal maintenance.

Early cannabinoid exposure influences neuroendocrine and reproductive functions in male mice: I. Prenatal exposure

Maternal exposure to Δ 9-tetrahydrocannabinol (THC), the major psychoactive constituent in marihuana, or to the non-psychoactive cannabinol (CBN) or cannabidiol (CBD) alters endocrine functions and concentrations of brain biogenic amines in their male offspring. Prenatal CBN exposure on day 18 of gestation resulted in decreased plasma FSH levels, testicular testosterone (T) concentrations, and seminal vesicles weights, but increased plasma levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) post-castration in adulthood. Prenatal exposure to THC significantly enhanced the responsiveness of the testes to intratesticular LH injection in vivo and tended to increase human chorionic gonadotropin (hCG)-stimulated T production by decapsulated testes in vitro. In the CBN-exposed mice, hCG-stimulated T production was enhanced, while CBD exposure had no effect. Prenatal THC exposure altered the negative feedback effects of exogenous gonadal steroids in castrated adults, with lower plasma T and FSH levels after 20 μg T than in castrated controls. In contrast, CBD-exposed mice had higher levels of LH in plasma post-castration. In CBN-exposed adults, two weeks post-castration the concentration of norepinephrine (NE) and dopamine (DA) in hypothalamus and remaining brain were reduced, while levels of serotonin (5-HT) and its metabolite, 5-HIAA, were elevated compared to that in castrated OIL-controls. Prenatal CBD-exposure also reduced NE and elevated 5-HT and 5-HIAA, but did not affect DA levels post-castration. Concentrations of brain biogenic amines were not influenced by prenatal THC exposure in the present study. A single prenatal exposure to psychoactive or non-psychoactive components of marihuana results in long term alterations in the function of the hypothalamo-pituitary-gonadal axis. Changes in the concentrations of brain biogenic amines may be related to these effects of prenatal cannabinoids on endocrine function in adult male mice.

17-α-estradiol and 17-β-estradiol in hippocampus

Electrophysiological field potentials recorded from in vitro hippocampal slice preparations show responses to exogenous gonadal steroids added to the incubation medium. The peak effect of the addition of 17-beta-estradiol occurred at a 100 pmol concentration; the CA1 field potential was increased by an average of 148 percent. 17-alpha-estradiol, often used as a negative control in experiments demonstrating estrogen specificity of receptor binding sites and biological responses, had no effect on field potentials following addition of drug to the incubation medium. The addition of a 100 pmol concentration of 17-beta-estradiol to the same slices which had been pretreated with 17-alpha-estradiol, blocked the facilitatory response elicited by the 17-beta-estradiol administered alone. Since no enhancement of the field potential is observed with 17-beta-estradiol following pretreatment of 17-alpha-estradiol, this would support the hypothesis that hippocampal modulation by gonadal steroid hormones may be due to involvement of an estrogen receptor mediated phenomena.

Effects of progesterone implants in the mesencephalon of ovariectomized rats on LH and FSH release triggered by exogenous gonadal steroids.

Unilateral implantation of crystalline progesterone into the caudal mesencephalic reticular formation (MRF) of chronically ovariectomized adult rats prevents the triggering effect of exogenous gonadal steroids on LH release and does not affect the release of FSH in the same animal.

Effects of gonadectomy and exogenous gonadal steroids on sex differences in open field behaviour of adult rats

Two experiments were carried out to investigate the contribution of gonadal hormones to the expression of sex differences in open field behaviour of adult female and male rats. In the first experiment rats were gonadectomized or sham-operated in adulthood and tested in the open field 1, 2, 3, 4, 5 or 6 weeks later (3 min/rat on 3 consecutive days during the light period of the day). It was found that following gonadectomy the well known sex difference in ambulation and rearing behaviour (females more than males), as well as in defaecation (females less than males) remained. Ovariectomy caused a decrease in ambulation and rearing, with an increase in defaecation, whereas castration had no significant effect on ambulation and rearing, but also increased defaecation. Also an overall increase in ambulation and rearing was found: animals tested 5 and 6 weeks following the operation were significantly more active than animals tested at 1–4 weeks after the operation. In the second experiment female and male rats were gonadectomized and 7 weeks later they received a silastic implant containing testosterone (T), dihydrotestosterone (DHT), oestradiol (E 2), DHT plus E 2, or nothing (control condition). Four weeks after the implantation the animals were tested in the open field (3 min/rat on 3 consecutive days). An overall sex difference was found for ambulation (females more than males) and for defaecation (females less than males). The only effect of hormone administration was found in DHT-treated animals: lowest ambulation and highest defaecation compared to other hormone and control animals. No differences were found between the T, E 2, DHT plus E 2, and control animals. From these data it was concluded that endogenous gonadal steroids seem to play a minor role in the expression of sex differences in adult open field behaviour in the rat.

Update on the Male and Female Climacteric*

The gonadal steroids--estrogens and androgens--appear to have a mood-elevating, psychotonic effect. The improved sense of well-being and increased vigor probably is engendered by restoration of somatic efficiency and psychic equilibrium. 1. The male climacteric, as observed in a limited number of men, is associated with a low level of serum testosterone. The levels of follicle-stimulating hormone and luteinizing hormone are not elevated because estrogen concentration continues unaltered well into old age. Androgen replacement therapy often lessens fatigue, depression and headaches, and headaches, and improves libidinous drives. 2. In the aging female, many climatric symptoms other than those due to vasomotor instability were heretofore considered merely coincidental. Recent studies suggest that the metabolism of cerebral hormones is markedly influenced by endogenous and exogenous gonadal steroids. Thus, postmenopausal depression, headaches, and nervousness may be hormone-dependent symptoms. 3. The incidence of endometrial cancer is no greater and is probably less in estrogen-treated women than in women not treated with estrogen, if regular cyclic courses of an oral progestogen are added to the regimen.

Steroid feedback regulation of luteinizing hormone and follicle‐stimulating hormone secretion rates in male and female rats

The long‐accepted dogma of feedback control of luteinizing hormone (LH) and follicle‐stimulating hormone (FSH) secretion by gonadal steroids is reconsidered in this article in light of recent investigations in the rat, using radioimmunoassay measurements of both the steroids and the gonadotropins. The negative feedback control of gonadotropin secretion in the female rat has been studied by many approaches; in every case, LH and FSH appear to respond differently to either removal or administration of gonadal steroids. Serum FSH increases rapidly after removal of one or both ovaries, but its secretion cannot be completely suppressed by any combination of exogenous gonadal steroids. LH secretion shows a delayed increase after ovariectomy or hemiovariectomy, but serum levels are readily suppressed by estradiol administration. Furthermore, the delayed increase in LH after ovariectomy corresponds more closely to the delayed drop in estradiol levels than does the rapid increase in FSH. Serum FSH secretion in the...

Development of capacity to secrete progesterone-induced protein by the porcine uterus.

Prepubertal gilts at various ages were treated for 15 days with gonadal steroids (estradiol and progesterone). On Day 15 the uteri were flushed with buffered saline to recover the secreted protein. The protein recovered was quantitated and analyzed by polyacrylamide gel electrophoresis. In a series of experiments it was found that gilts do not possess the ability to respond to exogenous gonadal steroids by secreting a complete adult pattern of uterine specific proteins until about 140 days of age. A partial pattern of uterine specific proteins was observed from about 112 days of age. This indicates that the ability to secrete all uterine specific proteins is not developed at the same time, but rather occurs during the period from 4 to 5 months of age. Even when gilts were able to secrete the entire pattern, the quantity of induced protein was normally much less than that in mature gilts.