Sex differences,laterality, and hormonal regulation of androgen receptor immunoreactivity in rat hippocampus

Sex differences, laterality, and hormonal regulation of androgen receptor (AR) immunoreactivity in rat hippocampal CA1 pyramidal cells were examined using the PG21 antibody. Adult male rats were either castrated or sham-operated at least 2 weeks prior to sacrifice. Gonadally intact females were sacrificed on the day of proestrus. Animals received an injection of either testosterone propionate (TP) or vehicle 2 h prior to sacrifice. Within CA1, both the intensity of staining and the number of AR+ cells were assessed. AR immunostaining was detected in all the groups with marked variation among them. The overall ranking of staining intensity was: gonadally intact males > females given TP > castrated males given TP > females > castrated males given vehicle. The number of AR+cells within subregions of CA1 showed the same basic pattern: among control-treated animals, gonadally intact males have more than females, but castrated males have the least, and acute TP treatment increases the number in both sexes. The increased level of AR immunoreactivity in CA1 of castrated males following acute TP treatment suggests that testicular androgens in adulthood normally increase AR immunoreactivity there, producing a sex difference favoring males in gonadally intact animals. We also found a higher number of AR+ CA1 cells on the left than on the right, but only in gonadally intact males and in females given TP. These results suggest that a laterality of AR distribution in the rat hippocampus may lead to lateralities in hippocampal structure and function.     

Critical Periods of Sensitivity of Sexually Dimorphic Spinal Nuclei to Prenatal Testosterone Exposure in Female Rats

Male rats normally have more neurons than do females in two nuclei of the lumbar spinal cord, the spinal nucleus of the bulbocavernosus (SNB) and the dorsolateral nucleus (DLN). Female rats exposed to testosterone propionate (TP) on the 2 days of gestation (Days 18 and 19) when males normally experience a surge in plasma testosterone showed a maximal increase in both SNB and DLN neuronal number. TP exposure just prior to, or following, Days 18 and 19 led to smaller increments. Administration of a small (5 μg) dose of TP after birth, while having no effect by itself, synergized with prenatal TP to enhance the number of SNB neurons. DLN neurons were less responsive to postnatal TP. The somal and nuclear size of SNB, but not DLN, neurons was increased by perinatal TP. Paradoxically, the number of DLN neurons with large somas (1358 μm²or larger) was reduced by perinatal TP, a finding congruent with a previous report that females and feminized males have more of these large DLN neurons than control males. Our data suggest an exquisite sensitivity of the developing spinal nuclei to the timing of hormonal surges normally found in fetal males. Exposure to androgens during a brief prenatal period is needed to assure responsiveness to the low amounts of androgen circulating during neonatal ontogeny, when the process of sexual differentiation is completed.     

The reproductive pattern of male dusky salamanders (genus Desmognathus) is neither associated nor dissociated

Many seasonally breeding vertebrate species have an associated reproductive pattern: mating behavior, gonadal activity, and peak circulating androgen levels occur simultaneously. In these species, androgens influence the expression of male mating behavior. Other species have a dissociated reproductive pattern: mating behavior occurs at a different time than peak gonadal activity. In such species, it is hypothesized that mating behavior is not dependent on androgen levels [Crews, D., 1984. Gamete production, sex hormone secretion, and mating behavior uncoupled. Horm. Behav. 18, 22-28]. The salamander Desmognathus ochrophaeus mates in the spring and fall while spermatogenesis occurs during the summer, suggesting that it has a dissociated reproductive pattern and that androgens do not mediate mating behavior. To assess whether mating behavior is regulated by gonadal androgens, we castrated males to reduce endogenous androgens and implanted testosterone propionate (TP) to restore androgen levels. Castrated males mated significantly less than did control males. Castrated males given TP mated as much as control males. Compared to controls, circulating androgen levels (both testosterone (T) and dihydrotestosterone (DHT)) were reduced in castrated males and elevated in castrated males given TP implants. We also found that plasma corticosterone (CORT) levels were strongly and positively correlated with T levels. Together, these data indicate that, although spermatogenesis is dissociated in time from mating behavior, androgens are associated with the expression of mating. Thus, the associated-dissociated dichotomy does not adequately describe the reproductive pattern of D. ochrophaeus. We discuss the limitations of the associated-dissociated framework in clarifying hormone-behavior relationships in reptiles and amphibians.     

Sexual preferences of male hamsters (Mesocricetus auratus) for conspecifics in different endocrine conditions

The behavioral responses of sexually experienced male hamsters toward a pair of anesthetized conspecifics were investigated. Males spent significantly more time licking, sniffing, and mounting neonatally and adult castrated males than intact males. Adult castrated males receiving oil injections were preferred over castrates receiving exogenous testosterone propionate (TP). Ovariectomized females were preferred over intact males, adult castrated males, or spayed females receiving exogenous TP. It was concluded that the absence of an androgen-dependent factor(s) renders an animal more sexually attractive.     

Parental responsiveness is feminized after neonatal castration in virgin male prairie voles, but is not masculinized by perinatal testosterone in virgin females

We previously found a large sex difference in the parental responsiveness of adult virgin prairie voles (Microtus ochrogaster) such that most males are spontaneously parental, whereas most females are not. Because this sex difference is independent of the gonadal hormones normally circulating in adult virgin voles, the present study examined whether perinatal hormones influence the development of this sex difference. Males were treated prenatally (via their pregnant dam) with both the androgen receptor blocker flutamide (5 mg/day/dam) and the aromatase inhibitor ATD (1 mg/day/dam), or oil, for the last 2 weeks of gestation. Half of the subjects from each group were castrated on the day of birth and the other half received a sham surgery. As adults, intact males were castrated and all males received a silastic capsule filled with testosterone. Prenatal treatment with flutamide and ATD had no effect on males' behavior toward pups, but neonatal castration significantly reduced the percentage of males acting parentally. In a second experiment, females were exposed to testosterone propionate (TP; 50 microg/day/dam) or oil via their dam during the last 2 weeks of gestation. For the first neonatal week, half of the females from each group were injected with TP (1 mg/day) and the other half oil. As adults, females were ovariectomized and half from each group received a testosterone-filled capsule and the other half received an empty capsule. None of the perinatal TP treatments increased females' parental responsiveness, although females from all groups that received testosterone capsules as adults were highly parental. Therefore, although postnatal testicular hormones are necessary for high parental responsiveness in males, the behavior of females is not influenced by perinatal exposure to testosterone.     

Testosterone-induced aggression in adult female mice

Silastic implants of testosterone (T) and injections of testosterone propionate (TP) were used to study the effects of ovariectomy and androgen administration on the fighting behavior of adult female mice. A dose of T previously shown to hyperstimulate accessory organ growth in adult male castrates was sufficient to induce the complete behavioral repertoire of male-like aggression in females never before treated with exogenous androgen. As determined by radioimmunoassay, blood levels of T produced by implants containing an aggression-inducing dose of T (10-mg implant) were within the range of T concentrations observed in intact males. Following treatment with a 10-mg T implant, the aggressive behavior of ovariectomized females could be fully maintained with a dose of T (0.3-mg implant) that failed to maintain weight of the accessory organs in adult male castrates. In fact, females “androgenized” were subsequently more responsive to the aggression-activating properties of T than were males castrated after prenatal and perinatal androgen exposure.     

Activation and differentiation of sexual behavior and translocation of hypothalamic estrogen receptors in rats by 6α-fluorotestosterone

Androgens classified as nonaromatizable in placental assay systems typically do not mimic testosterone's effects on sexual behavior in rats. 6α-Fluorotestosterone is an exception. To pursue this challenge to the aromatization hypothesis, we compared several behavioral and neuroendocrine effects of 6α-fluorotestosterone propionate (6α-fluoro-TP) with those of testosterone propionate (TP). Even at a very low dose (6.25 μg/100 g/day), 6α-fluoro-TP maintained most aspects of male sexual behavior as well as TP. It was slightly less potent than TP for inhibiting gonadotropin secretion (testicular development) in prepubertal males. Given neonatally, these androgens were equally likely to induce anovulatory sterility. 6α-Fluoro-TP defeminized sexual development in females and neonatally castrated males half as effectively as TP based on lordosis:mount ratios following estrogen and progesterone therapy in adulthood. Neither androgen masculinized sexual behavior. The behavioral effects of 6α-fluoro-TP correspond to its ability to inhibit cell nuclear accumulation of 17β-[³H]estradiol in the hypothalamuspreoptic area. When injected on a schedule like that used to activate male sexual behavior, the two androgens reduced estrogen uptake equally. When injected into adult castrates on a schedule like that used to defeminize sexual development, 6α-fluoro-TP blocked estrogen uptake half as well as TP. 6α-Fluorotestosterone did not alter estrogen uptake when injected simultaneously with 17β-[³H]estradiol. These data suggest that 6α-fluorotestosterone activates male behavior and defeminizes development because it translocates estrogen receptors in the brain, probably via an aromatized metabolite. Hence androgen aromatizability in the placenta may not reflect neural metabolism and cannot predict the behavioral or neuroendocrine effects of androgens.     

Effects of androgen on fighting behavior in male and female Mongolian gerbils (Meriones unguiculatus)

Contrary to the results of most other mammalian species studied thus far, castration in infancy or adulthood has been shown to increase the display of intermale aggression in gerbils tested as adults in dyadic encounters. Males castrated in adulthood were divided into two groups: one that received testosterone propionate (TP) treatment and one that did not. A third group of adult males were sham-operated. Infant subjects were either sham-operated or castrated and tested once without and once with TP. Both infant and adult castrates that received no TP treatment demonstrated significantly more fighting behavior than did sham-operates. Adult subjects treated with TP show significantly less aggression than castrates that did not receive TP. Ovariectomized females were also divided into a TP and no-TP group. Females treated with TP showed significantly less aggression than those that had no treatment showing that TP inhibits aggression in both males and females gonadectomized in adulthood. The results are assessed in terms of the importance of perinatal androgen to “organize” adult behavior patterns.     

Expression of male-typical behavior in adult female pseudohermaphroditic rhesus: Comparisons with normal males and neonatally gonadectomized males and females

Two types of pseudohermaphroditic female rhesus produced by exposure to either testosterone propionate (TP) or dihydrotestosterone propionate (DHTP) prior to birth were ovariectomized postpuberally and evaluated for the display of male-typical sexual behavior in response to exogenous TP in adulthood (2 mg/kg/day for 12 weeks). Their performance in standardized tests with estrogenized female partners was compared to that of neonatally gonadectomized males and females identically tested and treated with exogenous TP as adults. In addition intact adult males not given exogenous TP were tested with the same estrogenized female partners. There were no reliable differences between the two types of pseudohermaphrodites on any measure of behavior shown during the tests. Accordingly results were combined. Reliable behavioral changes induced by the TP given in adulthood were limited to increases in purse-lip responses, the induced increases were similar in pseudohermaphrodites and castrated males, and increases were reliably greater in these two groups of subjects than in females. Pseudohermaphrodites and castrated males did not differ reliably from intact males in performance of purse-lip gestures during TP treatment. In the performance of mounting, however, pseudohermaphrodites and castrated males remained consistently below the standard of the intact males. The estrogenized female partners displayed proceptive responses most frequently to the intact males and least frequently to the females. Their proceptive responses with castrated males resembled their performance with intact males, but with pseudohermaphrodites their proceptive responses more closely resembled their performance with females. Receptive behavior of the female partners was displayed most frequently to intact males, at intermediate levels to castrated males, and least often to pseudohermaphrodites. Results are completely consistent with the notion that androgens in high concentrations before birth alter mechanisms related to the later display of masculine behavior. These alterations in behavioral mechanisms are of such a nature that the display of male-typical behavior induced by androgens in adulthood is more pronounced and more frequent than it would have been otherwise. The alterations in masculine behavior observed in pseudohermaphroditic rhesus are not different in kind or scope than those reported extensively for lower mammals.(ABSTRACT TRUNCATED AT 400 WORDS)     

Androgenic stimulation of aggression eliciting cues in adult opponent mice castrated at birth, weaning, or maturity

The developmental and concurrent effects of androgens on aggression-eliciting qualities of male opponent mice were investigated during paired contests with trained fighters. Groups of male mice were castrated at either 1, 20, or 110 days of age. Half of each group were injected from 110 days of age with a maintenance dose of 100 αg testosterone propionate (TP), while the rest received injections of the arachis oil vehicle. The level of aggression received from fighter mice was monitored after 20 injection days, and compared to that received by intact male, and spayed TP-injected female opponents. The age at castration did not affect the responsiveness of opponents to androgens, and all TP-injected males suffered more severe defeat than oil-injected controls. TP-injected castrate males did not differ from intact males as opponents eliciting aggression, though TP-treated females received significantly more bites than any of the male opponent groups. A concurrent stimulation by androgens of the adult males' aggression-eliciting cues was, therefore, demonstrated. It is suggested that females derive different metabolic end-products from testosterone propionate, which can apparently provide more effective aggression-eliciting cues than are produced by the male mouse.     

Sexual differentiation of the steroid feedback mechanism regulating follicle-stimulating hormone secretion in the Syrian hamster

The ability of gonadal steroid hormones to influence tonic follicle-stimulating hormone (FSH) secretion was investigated in Syrian hamsters. In Experiment 1, males were castrated as adults, and administered testosterone in 20-, 30-, 40-, and 50-mm silastic capsules (s.c.) at 67, 74, 81, and 88 days, respectively. Circulating FSH was reduced by testosterone in a dose-dependent manner. A similar FSH response to testosterone in adulthood was evident in neonatally androgenized hamsters given testosterone proprionate (TP) on Days 0 and 1 of life. By contrast, the absence of gonadal androgens during the neonatal period (females ovariectomized at 60 days of age and males orchidectomized at birth) resulted in only a partial suppression of circulating FSH by even the highest dose of testosterone during adulthood. Treatment with estradiol benzoate at birth failed to produce a masculine response to androgen in adulthood. In Experiment 2, using a similar protocol, the nonaromatizable androgen, dihydrotestosterone, produced a dose-dependent suppression in serum FSH in males castrated in adulthood (30-, 60-, 90-mm capsules). However, dihydrotestosterone failed to alter the hypersecretion of FSH produced by orchidectomy at birth in males or in females ovariectomized at 60 days of age and treated neonatally with either vehicle or TP. In Experiment 3, treatment with estradiol (10-, 20-, 30-mm capsules) decreased serum FSH in gonadectomized hamsters in a dose-dependent manner; males and females treated neonatally with TP were more responsive to estradiol as adults compared to neonatally orchidectomized males or females treated with vehicle at birth.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of androgen pretreatments at adulthood on androgen-induced proliferative response of seminal vesicles in neonatally castrated mice

Male mice were castrated on days 0 and 60 after birth. The majority of the neonatally castrated mice were pretreated with androgen; the mice were given daily injections of testosterone propionate (TP; 4 or 8 micrograms/g body wt) for 20 or 30 days starting from day 60. Daily injections of TP (4 micrograms/g body wt) to examine androgen-induced proliferation were started from day 30 or 60 after the end of TP pretreatments or from day 60 after castration; on various days after starting TP injections, the weight and the incorporation of 5-[125I]iodo-2'-deoxyuridine into the whole seminal vesicles were determined as indices for proliferation. The seminal vesicles of neonatally castrated adult mice were characterized by long duration of androgen-induced proliferation (greater than 20 days) with a low peak (neonatal castration type), whereas the seminal vesicles of adult castrated mice were characterized by short duration of proliferation (10 days) with a high peak (adult castration type). In neonatally castrated adult mice, the neonatal castration type of androgen-induced proliferation was changed largely to the adult castration type when pretreatment with 8 micrograms/g body wt of TP had been given for 30 days. However, this effect gradually disappeared when the mice had been pretreated with decreasing amounts of TP for a shorter period. The present findings suggest that the defect in the androgen-induced proliferative response of mouse seminal vesicles induced by the absence of neonatal and prepubertal testicular androgens can be compensated by androgens given in adulthood, if enough androgen is given for a sufficiently long time.     

Effects of androgen administered to neonatal male rats on hypophyseal gonadotropin content, secretion and response to LHRH at adulthood

Supraphysiologic doses (1.75-3.50 mg) of testosterone propionate (TP) administered to male rats on the day of birth and 24 h later resulted in markedly reduced serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels in adult males castrated for 16 days. These effects diminished as androgen was injected on succeeding postnatal days. Since exogenous dihydrotestosterone and testosterone were similarly effective, aromatization to estrogen is not required to elicit these effects. No build-up of either gonadotropin occurred in the pituitaries of TP-treated animals; pituitary LH content was appreciably reduced, while FSH remained unchanged. These data imply that hypophyseal synthesis and secretion of gonadotropins are curtailed in adult castrated males who have been androgenized neonatally. Pituitaries of such neonatally treated animals, however, were capable of increased secretion of LH in response to a challenge of luteinizing hormone-releasing hormone. These findings are compatible with a model in which an androgen suppressible event occurs at a suprahypophyseal level, e.g., hypothalamus or higher brain centers, in the male rat during a restricted neonatal period, which is responsible for programming the development of mechanisms involved in accumulation and secretion of gonadotropins.     

Testosterone implanted in the preoptic area of male Japanese quail must be aromatized to activate copulation

Intracranial implantation of minute pellets of gonadal steroids was combined with aromatase inhibitor treatment to determine if aromatization within the preoptic area (POA) is necessary for androgens to activate sexual behavior in the Japanese quail (Coturnix japonica). In this species, implantation of pellets of testosterone propionate (TP) or estradiol benzoate (EB) in the POA of castrated males restores male-typical copulatory behavior. In Experiment 1, adult male castrated quail were implanted intracranially with 200-micrograms pellets of equimolar mixtures of crystalline TP + cholesterol (CHOL), TP + 1,4,6-androstatriene-3,17-dione (ATD, an aromatase inhibitor), EB + ATD, or CHOL and behavior-tested with intact males and females. Copulation was stimulated by POA implants containing TP or EB (three of six CHOL + TP males and two of seven ATD + EB males copulated vs zero of four CHOL males), but copulation was not inhibited by combining ATD with TP (three of four ATD + TP males copulated). In Experiment 2, adult male castrated quail were injected systemically with ATD or oil for 6 days prior to and 14 days after intracranial implantation of 200-micrograms pellets containing the same amounts of TP or EB as in Experiment 1. The ATD injections completely blocked copulatory behavior in males with TP implants in the POA such that ATD/TP and Oil/TP mount frequencies differed significantly, but failed to block copulation in males with EB implants in the POA (proportions of males copulating were ATD/EB, 6/8; ATD/TP, 0/6; Oil/TP, 4/7). The cloacal foam gland, an androgen-sensitive secondary sex character, was unaffected by the dose of ATD used. We conclude that activation of copulatory behavior by TP implants in the POA is not due to nonspecific effects of high local testosterone concentrations but rather to aromatization. These results support the hypothesis that cells within the POA aromatize testosterone to estrogens, which directly stimulate the cellular processes leading to activation of male-typical copulatory behavior.     

Differential expression of the tetracycline-controlled transactivator-driven human CYP1B1 gene in double-transgenic mice is due to androgens: application for detecting androgens and antiandrogens

Differential expression of the tetracycline-controlled transactivator (tTA)-driven human cytochrome p450 (CYP) 1B1 gene was found in the livers of male mice, at high levels in neonates, but at low levels in adults. The goals of this study were to determine whether the differential expression of the tTA-driven human CYP1B1 (hCYP1B1) gene in neonates and adults was testosterone dependent and whether flutamide, a representative potent antiandrogen, led to the induction of hCYP1B1. This was tested by treating castrated transgenic mice with testosterone propionate and musk extracts. It was concluded that: (i). the levels of expression of both tTA and hCYP1B1 gradually declined, with clear changes being apparent between 2 and 4 weeks of age, (ii). castration of adult males resulted in the increased expressions of both tTA and hCYP1B1 to levels similar to those found in adult females, (iii). treatment of castrated male and adult female mice with testosterone propionate and musk extracts led to the restoration of the levels of expression of hCYP1B1 in the adult males, and (iv). treatment of adult males with flutamide caused an increase in the levels of expression of hCYP1B1 in the adult females, as indicated by the antiandrogenic activity. Thus, the differential expression of the tTA-driven hCYP1B1 gene in the transgenic mice was caused by androgen, and it is possible that castrated male and adult female mice expressing the tTA-controlled hCYP1B1 could be used as the basis for a strategy for the detection of androgens and antiandrogens.     

Expression of adult female patterns of sexual behavior by male, female, and pseudohermaphroditic female rhesus monkeys

Gonadally intact pseudohermaphroditic female and normal female and neonatally castrated male rhesus monkeys were given estrogen treatment as adults and evaluated for attractivity, proceptivity, and receptivity during tests with a tethered stud male. Pseudohermaphrodites were produced by injecting their mothers during pregnancy with either testosterone propionate (TP) or dihydrotestosterone propionate (DHTP). Castrated males had reliably lower attractivity than normal females on all indicator responses shown by the tethered males. Additionally, castrated males showed reliably fewer proceptive responses on 4 of 5 measures than normal females. Receptivity could not be assessed in this situation for castrated males, because tethered males never contacted them unless the castrated males were displaying presentation. No reliable differences were observed between pseudohermaphrodites produced by prenatal treatments with TP or DHTP. Pseudohermaphrodites generally showed reliably less attractivity and proceptivity than normal females and reliably more of these traits than castrated males. Attractivity scores for pseudohermaphrodites were not different from those for normal females until proximity to the tethered male was established. Receptivity was not different in pseudohermaphrodites compared with normal females. Results indicate prenatal androgenization and its developmental sequelae lead to a defeminization in adulthood which, in this testing situation, was principally manifested by a deficiency in the performance of proceptive behaviors. Additionally, defeminization in rhesus monkeys, unlike that demonstrated in rodents, does not depend upon actions of an aromatizable androgen.     

Androgens and the social behavior of male and female lizards (Anolis carolinensis)

This study investigated the androgen specificity of aggressive and sexual behavior in the lizard Anolis carolinensis and the capacity of females of this species to exhibit male-typical copulation. Gonadectomized males and females were injected with testosterone propionate (TP) or dihydrotestosterone propionate (DHTP) or were implanted with Silastic tubing containing TP or DHTP. Either TP or DHTP activated male-typical sexual behavior in both males and females and activated aggressive behavior in males; DHTP activated aggressive behavior in females. Thus conversion of androgen to estrogen is not essential for these behavior patterns, and endogenous dihydrotestosterone may be important. TP but not DHTP stimulated receptivity in females, suggesting that conversion of testosterone to estrogen may underlie TP-stimulated receptivity. Females treated with TP did not differ from males in their display of male-typical courtship, neck-clasping, and intromission.     

Sex differences in the motor nucleus of cranial nerve IX-X in Xenopus laevis: a quantitative Golgi study

In the clawed frog (Xenopus laevis), motor neurons in cranial nerve nucleus IX-X control contraction of laryngeal muscles responsible for sexually dimorphic vocal behaviors. We examined sex differences in dendritic arbors of n.IX-X cells using the Golgi-Cox method. Three morphological classes of somal types (ovoid, triangular, and elongate) are present in similar frequencies in n.IX-X of both males and females. The male n.IX-X neuron is a more complex and hypertrophied version of the female n.IX-X cell. The number of primary dendrites is the same for both sexes, but males have more total dendritic segments. The overall dendritic length of male n.IX-X neurons is two to three times that of the female. Males have longer dendritic segments between all branch points. Male and female frogs differ in levels of circulating androgens; neurons of n.IX-X are targets for androgenic steroids. To determine if androgen can affect dendritic morphology in adult females, we examined Golgi-impregnated cells in n.IX-X from ovariectomized females treated with testosterone for 1 month. The total number of dendritic segments was reduced by androgen treatment due to reduction in the number of higher order dendritic segments; the number of primary dendritic segments was unchanged. Androgen treatment may induce resorption of higher order dendritic branches. The overall dendritic length of androgen-treated female n.IX-X neurons was unchanged, and dendritic segments were longer. Thus, although androgen can alter dendrites of n.IX-X cells in adult females, this short-term treatment does not produce a masculine dendritic architecture.     

Female-typical sexual behavior of rhesus and defeminization by androgens given prenatally

Adult rhesus monkeys were observed in standardized tests for female-typical sexual and related social responses. In the first experiment reported, 7 castrated males and 5 spayed females were paired with each of 4 intact males on two occasions following intramuscular injection with estradiol benzoate (EB) (6 micrograms/kg X 14 days) and on two other occasions without such treatment. In tests without EB, males and females did not behave differently toward the intact male partners, and all responses were displayed at low frequencies. In tests with EB, females showed reliably higher frequencies than males of approaching, sitting close to, grooming, and soliciting, and they presented to a higher proportion of the male partner's sexual contacts. EB reliably increased the frequency of display of all of these same five responses in females but not in castrated males. The intact male partners displayed reliably fewer approaches, sexual contacts, mounts, intromissions, and ejaculations to castrated males than to spayed females regardless of estrogenization. In a second experiment 10 intact adult pseudohermaphroditic females and 6 intact control females were tested following EB injections with each of the same 4 intact males. Pseudohermaphrodites were experimentally produced by injecting pregnant females with either testosterone propionate (TP) or dihydrotestosterone propionate (DHTP). Pseudohermaphrodites, regardless of type of androgen used in their production, showed reliably fewer solicits than controls to male partners. Moreover, they displayed most of the other responses at lower average frequencies than controls. Frequencies of intromission and ejaculation by intact male partners were reliably lower with pseudohermaphrodites than with control females, but frequencies of approach, sexual contact, and mount were not reliably different. We conclude that in this testing and measurement situation male and female rhesus monkeys differ markedly in the degree of expression of female-typical sexual behaviors, and genotypic males are behaviorally less responsive to estrogens than females. Exposing genotypic females to androgens during fetal life decreases the expression of female-typical, estrogen-influenced responses, and the effect is most pronounced on those soliciting responses that subserve proceptivity.     

Influences of pre- and postnatal testosterone treatment on defeminization of sexual receptivity in pigs

Sexual receptivity was evaluated in female and male pigs that had experienced varying periods of exposure to testosterone pre- and postnatally. For prenatal exposure, pregnant sows were treated with testosterone propionate (TP) from Day 29-35 or Day 39-45 of gestation at a dosage that caused virilization of the external genitalia of their female offspring. Eighty-three percent of the females that received TP prenatally had regular estrous cycles, but reached puberty later than control females. Only 26% of the females that received TP both pre- and postnatally (4-6 mo of age) were observed in estrus by 10 mo of age. After ovariectomy and acute treatment with estradiol benzoate (EB), the proportion of females that showed the immobilization response (receptivity) was similar for all groups of females independent of pre- or postnatal TP treatment. Females treated prenatally from Day 39-45 showed the immobilization response for fewer days after treatment with a high dosage of EB than did controls. On the basis of these observations, we conclude that receptivity in female pigs is not affected greatly by testosterone treatment at the stages of development that were investigated. Males castrated at birth and treated with a single injection of EB after 9.5 mo showed the immobilization response. In contrast, few males castrated at 8 mo or castrated at birth and treated with TP from 3 to 6 mo showed the immobilization response after EB treatment. These observations provide direct evidence for a postnatal component of testosterone-dependent defeminization of receptivity in male pigs.