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PubMed1978

Direct evidence that the arcuate nucleus-median eminence tuberoinfundibular system is not of primary importance in the feedback regulation of luteinizing hormone and follicle-stimulating hormone secretion in the castrated rat.

Adult rats which have received monosodium-L-glutamate (MSG, 4 mg/g BW) on alternate days for the first 10 days of life manifest central nervous system lesions largely restricted to the retina and the arcuate nucleus of the hypothalamus in which nearly 90% of the perikarya are destroyed, leaving axons in passage intact. In animals so treated, concentrations of dopamine within the arcuate nucleus and median eminence of the hypothalamus are reduced 52% and 57%, respectively, in males and 45% and 61% in females, whereas concentrations of norepinephrine in these same two areas are normal. Concentrations of both norepinephrine and dopamine in five other hypothalamic nuclei (dorsal septal, medial preoptic, suprachiasmatic, periventricular, and dorsomedial nuclei) are unchanged. Nevertheless, despite the destruction of the arcuate nucleus cell bodies of MSG-treated rats, postcastration levels of serum FSH and LH in males, and FSH in females were not significantly different from FSH and LH values in castrated controls. Serum LH in castrated, MSG-treated females was slightly but significantly lower than in castrated controls. It is concluded that the arcuate nucleus-median eminence tuberoinfundibular neurons are not of primary importance in the tonic, negative feedback regulation of gonadotropin secretion.

Animals↗
PubMed1978

Effect of castration and steroid replacement on immunoreactive luteinizing hormone cells in the pars tuberalis of the rat.

The response of LH cells in the pars tuberalis of the rat hypophysis to castration alone or castration and subsequent administration of testosterone propionate or estradiol benzoate was studied. To accomplish this, LH cells were labeled by the peroxidase-antiperoxidase immunocytochemical method, with use of an antiserum generated against hCG. LH cells were detected in the caudal region of the pars tuberalis of all intact control animals studied. After castration, LH cells in both the pars distalis and pars tuberalis showed similar degrees of hypertrophy and hyperplasia. This response was inhibited by either testosterone propionate or estradiol benzoate in the pars distalis as well as in the pars tuberalis. These results indicate that LH cells in the pars tuberalis, in addition to those in the pars distalis, are responsive to fluctuations in circulating steroid hormone levels and that the pars tuberalis may contribute to the overall secretion of gonadotropin by the adenohypophysis.

Animals↗
PubMed1979

Effects of sex steroid hormones on arginine vasopressin in intact and castrated male and female rats.

In the present study we have examined the effects of androgens and estrogens on circulating arginine vasopressin (AVP). Adult male Wistar rats had serum AVP levels of 0.4 microU/ml. Two weeks after bilateral castration, AVP rose to 2.6 microU/ml, but daily testosterone administration (100 microgram/100 g BW) to the castrate males prevented the AVP increase (0.8 microU/ml). During a normal estrous cycle, adult female Wistar rats had AVP values of 0.6 microU/ml during diestrus, 4.6 microU/ml on the morning of proestrus, 1.3 microU/ml on the afternoon or proestrus, and 1.5 microU/ml on the day of estrus. These changes in AVP paralleled the presumed changes in serum estradiol. Two weeks after bilateral ovariectomy of the adult female rats, AVP was 1.4 microU/ml but daily estradiol injections (100 microgram/100 g BW) to the castrate females produced a rise of serum AVP to 5.0 microU/ml. The results suggest an androgen inhibition and an estrogen stimulation of serum AVP levels.

Animals↗
PubMed1982

Heterogeneity of rat pituitary gonadotropins on electrofocusing; differences between sexes and after castration.

Anterior pituitary extracts from intact and 4 week postcastration male and female rats were electrofocused in sucrose density gradients within the pH range 3.5-10. Column fractions were combined to cover this pH range in 0.5 pH units and assayed for LH by in vitro bioassay and RIA and for FSH by radioreceptor assay and RIA. The pH distribution of bioactive LH was altered after castration in both sexes, with the proportion of recovered activity in the alkaline pH range increasing (P less than 0.01) from 52-57% in the intact animal to 71-73% after castration. In addition, significantly more bioactivity was recovered in the pH range 7-9.5 with the male (37%) than with either of the female (diestrous, 30% or proestrous, 28%) groups (P less than 0.05). FSH receptor binding activity was located in the pH region 3.5-6.5. Significantly less receptor binding activity was recovered in the pH range 3.5-4.5 with the female groups (39% and 37% diestrous and proestrous, respectively) than the male group (61%; P less than 0.05, P less than 0.01). The distribution of immunoreactive LH and FSH was similar to that observed with the LH in vitro bioassay and FSH radioreceptor assay. It is concluded that the charge distribution of pituitary gonadotropins is altered according to the sex of the animal and after castration. These findings provide further evidence that the type of gonadotropin produced by the pituitary is under endocrine control.

Animals↗
PubMed1983

Proliferative pattern of uterine cells from birth to adulthood in intact, neonatally castrated, and/or adrenalectomized mice, assayed by incorporation of [125I]iododeoxyuridine.

The proliferative pattern of uterine cells from birth to adulthood was investigated in mice. The uptake of 5-[125I] iodo-2'-deoxyuridine [( 125I]dUrd) by the whole uterus was used as an index of cell proliferation. Nearly parallel changes in uterine growth were found from days 0-25 after birth in both intact and neonatally castrated mice. In both groups of mice, the weight of the uterus increased (0.7-6 mg) and high [125I] IdUrd uptake values were found from days 0-15, while the weight remained nearly constant, and very low uptake values were found in the next 10 days. Additionally, we could demonstrate that adrenalectomy plus ovariectomy caused no significant effect on neonatal growth of the uterus. After day 25, the weight of uterus (6-50 mg) and [125I]IdUrd uptake increased again in the intact mice, but remained low in the neonatally castrated mice. The proliferative response of the uterine cells to exogenous 17 beta-estradiol was then examined. The injection of 17 beta-estradiol on days 0 (20 micrograms/mouse) and 10 (5 micrograms/mouse) induced significant increases in [125I]IdUrd uptake the next day. Neonatal castration had no significant effect on the responsiveness of the uterus to estrogen-induced growth in adult mice. These findings suggest that sex steroids secreted from both the ovaries and adrenals of neonatal and prepubertal mice play no significant role in the proliferation of uterine cells, and that a quiescent interval of cell proliferation occurs around day 20 after birth between the autonomous (days 0-15) and the ovary-dependent (after day 25) proliferation of mouse uterine cells.

Adrenalectomy↗
PubMed1975

Effects of acute stress on serum LH and prolactin in intact, castrate and dexamethasone-treated male rats.

The effects of handling, ether vapor anesthesia and blood sampling on serum LH and prolactin were determined in intact, castrate and dexamethasone-treated male rats. Cage removal and transport to an adjacent room increased LH and prolactin levels by 10 and 15 min after the initial animal disturbance. Intact male rats subjected to repeated ether anesthesia and blood sampling showed a more rapid increase in serum LH and prolactin than the preceding rats, since serum LH and prolactin was increased by 4, 8 and 15 min after initial cage disturbance. In a group of rats subjected to serial blood sampling over a longer time interval, both prolactin and LH levels remained higher than 90 min after initial animal handling. At 90 minutes after a single blood sampling, blood prolactin concentration remained higher than in controls. Serum LH levels returned to control levels 90 min after the stress of a single blood sampling. Although serum prolactin was increased in the castrate group subjected to serial anesthesia and blood sampling, LH concentrations were reduced under the same conditions. Injection of 5 and 50 mug of dexamethasone/100 g body wt for 8 days markedly reduced adrenocortical responsiveness to the stress of serial anesthesia and blood sampling at 1, 4, 8 and 15 min after initial rat disturbance. The 50 mug dexamethasone treatment reduced the stress-stimulated increase in serum prolactin at all blood sampling intervals. The dexamethasone-treated groups also showed smaller increases in serum LH at 8 and 15 min after first animal handling than the control rats. These results indicate that serum LH and prolactin concentrations are consistently increased by acute stress in intact male rats, the duration of the stress stimulation of LH and prolactin is at least 90 min under the conditions of this study, serum LH levels of castrate male rats are decreased by acute stress and dexamethasone administration lowers stress stimulation of LH and prolactin release.

Anesthesia↗
PubMed1975

The effects of castration on histamine levels and 24-hour rhythm in the male rat hypothalamus.

Holtzman male rats were castrated or sham-operated at 22 days of age and raised in a 12 h light: 12 h dark illumination cycle. At age 63 days they were sacrificed by decapitation at six different times during the light:dark (L:D) cycle, and hypothalamic histamine (H) concentrations were measured using a modified single isotope-enzyme microassay. Hypothalamic H was significantly elevated in the castrated rats at all but two of the six times sampled during the L:D cycle, when compared with the sham-operated controls. Both surgical groups had similar 24-h rhythms of hypothalamic H concentrations, with the peak concentration occurring during the light phase followed by a rapid drop to the minimum 2-3 h later. However, the castrated rats appeared to attain both maximal and minimal concentrations somewhat earlier in the day. These results provide circumstantial evidence that hypothalamic H may have a role in the hypothalamo-hypophyseal-gonadal axis in the male rat.

Aging↗
PubMed1975

The effects of Methallibure (ICI 33,828) on the LH release in castrate male rats challenged with LHRH.

Daily administration of 10 mg of Methallibure (ICI 33,828) for 6 days to male castrate rats resulted in significant depression of serum radioimmunoassayable luteinizing hormone (LH). Subsequent challenge with 100 ng of synthetic luteinizing hormone-releasing hormone (LHRH) showed these rats to release sufficient pituitary LH to achieve plasma levels equal to those of LHRH treated castrate controls. Although an effect at the level of the pituitary remains to be conclusively ruled out, these results suggest that the predominant in vivo effect of Methallibure in the castrate male rat is to suppress pituitary LH release due to diminished secretion of LHRH by the hypothalamus.

Animals↗
PubMed1975

Specific, high-affinity binding of 17beta-estradiol in cytosols from several brain regions and pituitary of intact and castrated adult male rats.

Specific 17beta-estradiol binding capacities of cytosols from several brain regions and pituitary were determined in intact and castrated adult male rats. The binding capacity of the pituitary was approximately 10 times higher than that of any of the 5 brain region studied. Of these brain regions, the highest 17beta-estradiol binding capacities were present in the anterior hypothalamus followed by progressively lower capacities in the posterior hypothalamus, amygdala, midbrain, and cerebral cortex. The specific 17beta-estradiol binding capacity of cytosol from the anterior hypothalamus was significantly higher in castrated males than in intact rats. No such difference was found in any of the other tissues studied. Using sucrose gradient ultracentrifugation, an 8S sedimentation coefficient was found for the specific estradiol binding macromolecules present in cytosols from pituitary as well as anterior and posterior hypothalamus of castrated rats. The affinity for estradiol of cytosols from anterior and posterior hypothalamus was very high, with the mean association constants being 2.9 and 2.4 X 10(10) M-1, respectively. In competition experiments the 17beta-estradiol binding molecules present in cytosols from pituitary and anterior hypothalamus showed a higher affinity for 17beta-estradiol than for either estrone or estriol. In both tissues these 17beta-estradiol binding molecules showed a moderate affinity for the anti-estrogens MER-25 and cis-clomiphene citrate as well as for the androgen 3beta-androstranediol, but almost no affinity for 3alpha-androstanediol, 5alpha-dihydrotestosterone, testosterone, or corticosterone. These findings suggest that a true cytoplasmic receptor for estradiol exists in the male rat brain and pituitary which may play an important role in regulating reproductive function.

Amygdala↗
PubMed1976

Effects of castration, testosterone, estradiol, and prolactin on specific prolactin-binding activity in ventral prostate of male rats.

Lactoperoxidase-catalyzed 125I-labeled ovine prolactin (PRL) was found to bind specifically to particulate membrane fractions of rat ventral prostate. Unlabeled PRL readily displaced the labeled PRL, whereas ovine GH, LH, FSH, or TSH showed no such competition. Castration reduced the binding of 125I-labeled PRL to about 1/6 of that in intact rats, and injections of testosterone propionate (TP) increased PRL binding to values as great or greater than those in intact controls. Injections of TP into intact immature and mature rats also increased PRL binding. In vitro binding of labeled PRL was inhibited in prostatic tissue removed from intact immature rats 2 h after injecting unlabeled PRL, but not in ventral prostates from rats killed 26 or 74 h after injecting unlabeled prolactin. PRL injected together with TP in castrated rats produced no greater increase in prolactin binding than TP alone, while estrogen appeared to decrease PRL binding beyond that produced by castration alone.

Animals↗
PubMed1981

Medical castration of males with megestrol acetate and small doses of diethylstilbestrol.

An alternative program for medical castration for treatment of prostate cancer has been developed using a progestational antiandrogen, megestrol acetate (MA), in combination with small doses of diethylstilbestrol (DES; 0.1 mg/day). The administration of MA (40-80 mg/day) with 0.1 mg DES to nine patients resulted in castrate levels of plasma testosterone (less than 0.4 ng/ml) and significant suppression of both FSH and LH (P less than 0.05) for up to 12 months. Although large clinical trials must ultimately establish its safety, clinical side effects of this combined therapy to date have consisted of mild gynecomastia in two patients. The symptoms did not necessitate discontinuing the medications. It is concluded that the use of 0.1 mg DES with a minimum of 40 mg/day MA results in medical castration with sustained suppression of plasma testosterone. Because of the possible additional therapeutic advantage of blockade of intracellular androgen-mediated action by MA in androgen-dependent tumors, this combined therapy should be further explored as a possible initial treatment of choice for advanced prostate cancer.

Castration↗
PubMed1982

Estrogen-dependent plasma prolactin response to gonadotropin-releasing hormone in intact and castrated men.

Although it has been recently shown that GnRH is capable of increasing plasma PRL levels in humans, the role played by the steroid hormone environment in influencing this response has not been clarified. Fourteen intact and 14 castrated subjects with carcinoma of the prostate were studied before and after daily treatment with 1.5 mg estradiol benzoate (E2B), im, for 9 days PRL responsiveness was tested after GnRH was given as an iv bolus or a continuous infusion for 4 h. During a 4-h saline infusion after E2B treatment, plasma PRL levels were measured in 8 intact and 8 castrated subjects for control purposes. No significant increase in PRL levels was noted after iv bolus or infusion of GnRH in intact or castrated men. After the administration of pharmacological doses of E2B for 9 days, plasma PRL levels increased significantly in all subjects after both the iv bolus and the infusion of GnRH. During saline infusion, a significant decrease in plasma PRL levels was observed in all subjects. Plasma gonadotropin levels showed the expected increase after GnRH administration. Our findings confirm that GnRH is one of the numerous substances capable of stimulating PRL release in humans and demonstrate that in men: 1) pharmacological doses of estrogen induce a PRL response to GnRH, and 2) GnRH elicits different patterns of PRL release depending on the modality of administration. Finally, the physiological role of GnRH in PRL release, if any, remains to be established.

Aged↗
PubMed1983

Male sexual development in the monkey. II. Cross-sectional analysis of pulsatile hypothalamic-pituitary secretion in castrated males.

Pulsatile secretion of serum gonadotropins was studied in 16 castrated monkeys from 4 weeks of age through adult life. Animals were castrated at various ages from birth through adult life. Although some studies of the gonadotropin-secretory patterns were longitudinal in nature, most comparisons were cross-sectional. On the basis of our observations, we have arbitrarily grouped the animals into 4 developmental ages: postnatal (less than 7 months), prepubertal or juvenile (7-27 months), pubertal (28-59 months), and adult (greater than or equal to 60 months). In carrying out these studies, blood was withdrawn at 15-min intervals over 24 h without anesthesia using a mobile vest and tether assembly to support an indwelling catheter. GnRH challenge tests were done on 1 or more occasions on all animals. Plasma samples were analyzed for concentrations of FSH and LH by established RIAs and an in vitro bioassay for LH. During the frequent sampling period (24 h for all except postnatal animals), the amplitude of gonadotropin pulses was greatest in adult animals followed by postnatal and pubertal monkeys. During pubertal development, there was a marked increase in the magnitude of gonadotropin pulses, and remarkedly, there was a substantial increase in the LH bioassay: RIA (greater than 5:1) by adult life. GnRH challenge tests of gonadotropins correlated with these observations. Time series analysis was applied to the data for objective statistical characterization of cyclic patterns. Our findings can be summarized: 1) during pubertal maturation there is a change in amplitude but not frequency of gonadotropin pulses, 2) pubertal development of the hypothalamic-pituitary axis advances in the absence of gonadal feedback, and 3) there is a significant increase in the LH bioassay: RIA during pubertal development. We conclude that the castrate monkey is a valuable adjunct to direct clinical investigations of the mechanisms controlling human sexual development.

Age Factors↗
PubMed1984

Inhibition of basal and adrenocorticotropin-stimulated plasma levels of adrenal androgens after treatment with an antiandrogen in castrated patients with prostatic cancer.

The basal plasma levels of cortisol, dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), and testosterone were studied in 20 patients with advanced prostatic cancer receiving combined treatment with an LHRH agonist and an antiandrogen [5,5-dimethyl-3-[4-nitro-3-(trifluoromethyl)-phenyl]-2 4-imidazolidinedione]. After 60 days of combined antihormonal therapy, plasma levels of testosterone decreased from 5.44 +/- 0.44 (SEM) to 0.136 +/- 0.052 ng/ml (2.5% of control). Somewhat unexpectedly, the plasma concentrations of the adrenal androgens DHEA and DHEA-S were reduced to 45 +/- 7 and 64 +/- 4% of control, respectively. The maximal reduction in plasma adrenal androgen levels occurred between 2 and 4 weeks of treatment. Whereas the increase in serum cortisol, 17-hydroxypregnenolone, and 17-hydroxyprogesterone concentrations 2 1/2 h after the injection of 0.25 mg human ACTH 1-24 was not affected by the combined treatment, the increment of DHEA and androstenedione after the same stimulus was reduced from 3.1 +/- 0.98 and 0.73 +/- 0.11 to 1.48 +/- 0.5 and 0.31 +/- 0.05 ng/ml, respectively. The reduced levels of serum DHEA and DHEA-S were not due to the LHRH agonist by itself, since similarly low levels of serum DHEA and DHEA-S were found in patients surgically castrated and receiving the same antiandrogen. These data suggest that treatment with an antiandrogen in castrated men inhibit the formation of adrenal androgens due to a blockade at the level of 17, 20-desmolase. The efficiency of the new combined antihormonal therapy (castration and antiandrogen) aimed at complete androgen neutralization in prostate cancer is thus further facilitated.

Adrenocorticotropic Hormone↗
PubMed1980

[The in vivo metabolism of chlormadinone acetate in guinea pig and the uptake of testosterone-3 H and chlormadinone acetate-3 H in prostate of castrated male rat (author's transl)].

The metabolic fate and distribution of the anti-androgenic agent, 17 alpha-acetoxy-6-chloropregna-4, 6-diene-3, 20-dione (chlormadinone acetate, CMA), was investigated using guinea-pigs and rats. In order to elucidate the metabolic outcome, chlormadinone acetate was labelled with 3H at position C-1 and with deuterium at methyl moiety of the 17alpha-acetate. Guineapigs were maintained for 7 days on a diet containing 1% chlormadinone acetate having a ratio of d2/d0=1 and then for 1 day on a diet containing 1% chlormadinone acetate having radioactivity. The isolation and purification of the urinary and fecal metabolites were usually carried out in the manner shown in Fig. 1 and 2. The metabolites identified were as follows: the parent drug, monohydroxychlormadinone acetate having the additional hydroxy function in the steroid skeleton, 15 beta-hydroxy, 2 alpha-, 2 beta-hydroxy and unknown position, dihydroxy chlormadinone acetate, 2 alpha-, 3 beta-dihydroxy, 2 alpha-, 3 alpha-dihydroxychlormadinone acetate. Further, three dechlornated and reduced metabolites were also isolated from urine and feces. These were 17 a-acetoxy-5a-pregnane-3 beta-ol-20-one and its isomer, and 17-acetoxy-5 beta-pregnane-2 beta, 3 beta, 15a-triol-20-one. But 3 beta-hydroxychlormadinone acetate possessd with anti-androgenic activity, one of the main metabolites in humans and rats, was not found in the excreta of the guinea-pigs. However, the main metabolite on the prostate of the guinea-pigs and rats and 3 beta-hydroxychlormadinone acetate. Chlormadinone acetate causes regression of the seminal vesicle and prostate in oral administration to a mammalian. It was therefore hypothesized that chlormadinone acetate might inhibit the uptake and retention of testosterone in these tissues. To elucidate this hypothesis, the accumulation of testosterone-3H and chlormadinone acetate-3H in several organs was determined on castrated rats and normal rats, respectively. When 1.0 muM of testosterone-3H was given to the castrated rats, a maximal accumulation of radioactivity resulted in seminal vesicle and prostate at 15 approximately 120 min. While the treatment of chlormadinone acetate significantly prevented the accumulation of testosterone-3H in the seminal vesicle and prostate, but levels in fat and muscle were not evident. In addition, to prove the accumulation of chlormadinone acetate in androgen target tissues, 3 muM of chlormadinone acetate-3H was similarly administered to castrated rats. The uptake of chlormadinone acetate on the target organs was higher than that in normal rats at 5 approximately 30 min.

Animals↗
PubMed1984

[Longitudinal studies on gonadotropin levels in patients with Turner's syndrome and patients with prepubertal castration].

Basal and LH-RH induced plasma FSH and LH levels were determined longitudinally in 41 patients aged 4 to 22 years with Turner's syndrome and in 4 male patients with prepubertal castration. In 12 patients with Turner's syndrome over 18 yrs of age without pubertal change, basal and LH-RH induced FSH levels studied at age 11--22 yrs were all significantly increased over normal levels. However, some of these patients had normal basal and LH-RH induced LH levels. In 5 patients with mosaic Turner's syndrome with spontaneous puberty, basal and LH-RH induced FSH and LH levels studied at age 6--12 yrs were always within the normal range for age-matched controls. In 10 patients studied at age 11--18 yrs, basal and LH-RH induced FSH levels were also strikingly increased over normal levels except for one patient. This patient had normal basal FSH and LH levels and serum estradiol level was increased from 49 to 199 pg/ml after HMG test. In 14 patients aged 4--10 years, nine patients had elevated basal FSH levels and abnormally high responses to LH-RH. The remaining 5 patients had normal basal FSH levels, and 3 of them also had normal FSH responses to LH-RH. The data on the 5 patients studied again at the age of greater than 13 yrs rose to high levels in adult castrated ranges. In 24 patients aged 4 to 17 years, 23 patients were thought to have no ovarian function, and one was thought to have spontaneous puberty. In 4 male patients with prepubertal castration, basal and LH-RH induced FSH levels were increased over normal levels after 11 yrs of age. However, basal LH levels in some patients were within the normal range for age-matched controls after 12 yrs of age. From these results, we conclude that basal and LH-RH induced FSH levels may provide definitive evidence of absent ovaries or testes in patients over 11 yrs of age with primary hypogonadism.

Adolescent↗
PubMed1975

Differential effects of castration on LH and FSH secretion in male and female rats.

Serum levels of LH and of FSH have been measured using specific radioimmunological procedures in normal controls and in male and female rats submitted to castration 1, 2, 7, 14, 21, 28 and 35 days before. Gonadectomy is followed by a rapid increase of serum levels of LH in males, and by a delayed response in females. The responses of serum FSH to castration are quantitatively and qualitatively similar in the two sexes. Both in males and in females an elevation of serum FSH levels is already present 1 day after the operation. Serum FSH continues to rise, between post-castration days 1 and 7 with a rather rapid slope, and at later intervals with a smoother progression.

Animals↗
PubMed1978

Sex differences in catecholamine content in discrete brain nuclei of the rat: effects of neonatal castration or testosterone treatment.

Dopamine and norepinephrine levels were measured in individual brain nuclei in normal adult male and female rats and in adult male rats castrated on day 1 of life and in adult female rats given 1.25 mg testosterone propionate on day 4 of life. Normal adult males showed higher concentrations of dopamine than females in the caudate, tractus diagonalis and arcuate nuclei and in the median eminence. Day 1 castration of males reduced the dopamine levels of the arcuate nucleus and nucleus of the tractus diagonalis, while neonatal administration of testosterone to females elevated the dopamine concentration of the arcuate nucleus and nucleus of the tractus diagonalis. Normal adult males had higher concentrations of norepinephrine than females in the preoptic-suprachiasmatic, paraventricular, periventricular, and arcuate nuclei and in the median eminence. Neonatal endocrine manipulations (neonatal male castration and female testosterone treatment) failed to alter significantly these sex differences. The results suggest a sexual dimorphism in the catecholamine innervation of certain discrete areas of the brain and that the dopamine concentration in the arcuate and tractus diagonalis nuclei is influenced by perinatal androgen.

Animals↗