Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Masculinity”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,351 records · Page 75Linked to original sources
PubMed1985

Luteinizing hormone-releasing hormone facilitates the display of sexual behavior in male voles (Microtus canicaudus).

To investigate whether luteinizing hormone-releasing hormone (LHRH) influences the sexual behavior of male gray-tailed voles (Microtus canicaudus), subcutaneous injections of LHRH (500 ng) were given to intact males and to castrated males with different levels of testosterone replacement. Intact voles, as well as castrated voles with Silastic capsules of testosterone propionate, showed significant facilitation of several parameters of masculine sexual behavior 2 hr after LHRH injection, compared to saline controls. Castrated voles without testosterone replacement showed no sexual behavior, even when injected with LHRH. These results support the hypothesis that LHRH regulates sexual behavior in M. canicaudus and that the behavioral response to LHRH is dependent on testosterone. The specific behavioral parameters affected suggest that LHRH changes the arousal component of masculine behavior in voles.

Animals↗
PubMed1985

Estrogens before birth and development of sex-related reproductive traits in the female guinea pig.

Influences of estrogens on the differentiation of psychosexual traits in the female guinea pig were studied. Pregnant animals were injected intramuscularly with either 1, 2, or 3.3 micrograms estradiol benzoate (EB) or with 1 or 3 micrograms diethylstilbestrol dipropionate (DESDP). Injections were started on the 29th day of pregnancy, given daily for 6 days, and continued every other day until parturition. Female offspring were evaluated for onset of puberty, ovarian function, and lordosis and mounting behavior in adulthood. Prenatal treatment with 3 micrograms DESDP caused delayed puberty, impaired ovarian function, reduced responsiveness of lordosis to EB and P in adulthood (defeminization), augmented mounting in the absence of hormones (masculinization), and reduced responsiveness of mounting to exogenous EB and P in adulthood (defeminization). Prenatal treatment with 1 microgram DESDP produced similar but less pronounced effects. Prenatal treatment with 3.3 micrograms EB also caused a delay in puberty. However, responsiveness of lordosis to EB and P in adulthood was enhanced by treatment with either 1 or 3.3 micrograms EB prenatally. Further, neither mounting in the absence of hormones nor mounting in response to EB and P in adulthood were affected in any measurable way by any prenatal treatment with EB. These results show that estrogens can have masculinizing and defeminizing effects on sexually dimorphic reproductive traits in guinea pigs. The failure of EB to duplicate or parallel the effects of DESDP is not completely understood at this time, but it may indicate that less of the active substance reaches the target tissues following maternal and placental metabolism of EB than of DESDP.

Animals↗
PubMed1986

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)

Animals↗
PubMed1982

Sex differences in aortic cholesterol esterase activity in rats, and changes of the activity following castration and gonadal hormone treatment.

Sex differences in aortic cholesterol esterase activity and changes in the activity following castration and gonadal hormone treatment were investigated in rats. Differences in the enzyme activity were apparent after 2.5 months and became most significant after 6 months. The activity in the aorta and the liver was significantly higher in female rats. Prepubertal orchiectomy increased the aortic activity, feminizing the type of metabolism, whereas postpubertal orchiectomy, and both pre- and postpubertal ovariectomy induced no change in the activity. The administration of testosterone to female rats significantly decreased the aortic activity, masculinizing the type of metabolism. However, the administration of testosterone or of 17 beta-estradiol to male rats had no effect. These results suggest (1) that there are clear sex differences in aortic cholesterol esterase activity, (2) that prepubertal exposure to androgens plays a critical role in the sexual differentiation in aortic and hepatic cholesterol ester metabolism, and (3) that the administration of testosterone can temporarily masculinize the type of metabolism. These results partly explain the sexual differences in susceptibility to atherosclerosis.

Aging↗
PubMed1983

Male pseudohermaphroditism due to 17 beta-hydroxysteroid dehydrogenase deficiency: studies on the natural history of the defect and effect of androgens on gender role.

Studies within the Arab population in Israel revealed 25 pseudohermaphrodites due to 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) deficiency. Twenty-three individuals, presently living in the Gaza strip, belong to a very large inbred kinship which extends over 8 generations. All affected subjects (46, XY) were born with mild to moderate degrees of ambiguity of an apparently normal-looking female genitalia and therefore were reared as girls. In childhood, genital abnormalities consisted of a clitoral-like phallus surrounded by a chordee, non-fused labial-scrotal folds and a urogenital sinus. The testes were in the inguinal canals, or rarely, in the labial-scrotal folds. Wolffian structures were normally differentiated while Mullerian structures were absent. At puberty, subjects developed a male body habitus with abundant body hair and beard. Gynecomastia was absent. The phallus and testes enlarged to adult proportions while the prostate remained small. Together with the physical change from girls to boys they developed a male identity having erections and ejaculations, which in 7 cases led to the spontaneous adoption of a male gender role. In adults the hormonal abnormalities consisted of greatly elevated delta 4-androstenedione (delta 4) (350-1267 ng/dl) associated with subnormal testosterone (T) levels (0.9-3.1 ng/ml). Dihydrotestosterone (DHT) levels, with the exception of 1 patient, were relatively low in all cases (27-35 ng/dl). Children had low levels of delta 4, T and DHT, which were normal for age. Although from puberty on there was a significant rise of the 3 androgens, delta 4 always remained extremely elevated and T and DHT relatively low when compared to normal controls. Dexamethasone failed to suppress the androgen pattern while HCG augmented the defect, making the diagnosis possible in 2 prepubertal children. Dehydroepiandrosterone (DHEA) and 17-hydroxyprogesterone (17-OHP) levels were normal or moderately elevated. Estradiol (E2) levels were normal in children and all but 2 adults, who had high levels. LH and FSH levels were very high after puberty, but normal before. However, there was an overresponse to LHRH in all age groups. The contrast between the lack of intrauterine virilization of the external genitalia in fetuses with 17 beta-HSD deficiency versus the marked masculinization that occurs after puberty still remains a puzzling phenomenon. It is conceivable that the postpubertal development of a male phenotype with change of gender identity and role occurs due to the joint effect of delta 4, T and DHT, even though secreted in inadequate proportions. Thus masculinization in these individuals is a slow process requiring a longer period of time than that of normal puberty to be completed.

17-Hydroxysteroid Dehydrogenases↗
PubMed1987

The influence of gonadal steroids and the pituitary on the levels and composition of plasma phospholipids in the rat.

Gonadal steroids have been shown to influence plasma phospholipids. In the present study, the possible interaction between gonadal steroids and the pituitary in the regulation of plasma phospholipids was studied in rats. The total phospholipid concentration (higher in females) and the fatty acid composition of plasma lecithin was different in male compared to female rats. Gonadectomy resulted in a "feminization" of plasma phospholipids (total concentration and fatty acids in lecithin) in male rats but had no effect in females. Testosterone treatment of gonadectomized males or intact females resulted in a "masculinization" of plasma phospholipids, whereas estrogen treatment of intact males resulted in a "feminization." Hypophysectomy resulted in a marked decrease in plasma phospholipid concentration and the fatty acid composition of lecithin showed a "masculine" pattern in both males and females. Neither testosterone nor estrogen treatment had any effects on plasma phospholipids in hypophysectomized male and female rats, respectively. It is concluded that gonadal steroids and the hypothalamic-pituitary axis interact in the regulation of the synthetic and perhaps also degradative pathways controlling plasma phospholipids.

Animals↗
PubMed1991

Effects of social stress and intrauterine position on sexual phenotype in wild-type house mice (Mus musculus).

Wild-type house mice were used to test the effect of intrauterine position on anogenital distance (AGD) and to verify whether crowding stress would masculinize female pups, developing at all intrauterine positions, as has been demonstrated in CF-1 mice stressed by restraint, heat, and light. Stress of crowding was documented by comparing aggressive behavior, litter birth weights, and plasma corticosterone levels among females in different densities. AGDs were recorded from pups born to females housed from day 12 to 19 of gestation either individually with their mate (nonstressed) or in one of two group-housed densities. Female pups from nonstressed dams positioned between two males in utero (2M females) had longer AGDs than females positioned between two females (0M females). AGDs of males from nonstressed dams did not differ on the basis of intrauterine position. Group-housed pregnant females in the higher of two densities had female pups with longer AGDs than female pups of other dams. However, variance in female pup AGD was no different among dams in different densities. These results extend to the wild house mouse previous findings in albino mice that intrauterine position influences sexual phenotype. In addition, social stress can induce masculinization of female pups in wild mice as physical stress has been shown to do in albinos. This suggests that intrauterine position effects and their modification by crowding stress can potentially influence the dynamics of wild house mouse populations.

Aggression↗
PubMed1992

Lesions of the medial amygdala produce severe impairment of copulatory behavior in sexually inexperienced male rats.

The effects of amygdaloid lesions on masculine copulatory behavior were examined in male rats. Sexually inexperienced male rats were castrated and subjected to bilateral lesions in one of the following areas: the medial amygdala, the cortical amygdala, or the basolateral amygdala. Three weeks later, all rats received implantation of silastic capsules containing testosterone. Then, four observations of copulatory behavior were carried out every 5 days following the implantation of testosterone. Rats with medial amygdala lesions showed a severe deficit of copulatory behavior, whereas rats with basolateral amygdala lesions showed no change in the performance of copulation. As for rats with cortical amygdala lesions, although their copulatory behavior was impaired, the effect was confined to a deficit in intromission and ejaculation responses. These findings suggest that the medial amygdala plays a critical role in regulating masculine sexual behavior in the rat.

Amygdala↗
PubMed1993

Microinjection of galanin into the medial preoptic nucleus facilitates copulatory behavior in the male rat.

The medial preoptic area (MPOA) is an important region for masculine sexual behavior. Because galanin (GAL) immunoreactive cells within the MPOA are affected by the gonadal steroid environment and GAL binding is apparent, GAL was microinjected site specifically in 0, 10, 50, 100, and 500 ng doses in order to determine effects on copulatory behavior. Unilateral microinjection of GAL within the medial preoptic nucleus facilitated copulatory behavior in a dose-responsive fashion, evidenced by an increase in the percentage of males that displayed sexual behaviors and a decrease in mount and intromission latencies. These effects required the presence of gonadal steroids, and were not due to general arousal as measured in open field testing. The techniques of survival analysis were used to display data and for statistical analysis of intromission and mount latencies; these approaches revealed significant effects that were not evident with more commonly used procedures. The results support the suggestion that sexually dimorphic galaninergic cell groups within the MPOA are involved in gonadal steroid-induced masculine sexual behavior.

Animals↗
PubMed1996

Inhibition of male sex behavior by androgen receptor blockade in preoptic area or hypothalamus, but not amygdala or septum.

Inhibition of masculine copulatory behavior was previously demonstrated following systemic injections of hydroxyflutamide (OHF). In the present study, we examined the localization of the effects of this androgen receptor blocker by direct intracranial implantation of OHF into the medial preoptic area (MPOA), ventromedial nucleus of hypothalamus (VMN), medial amygdala (AME), and lateral septum (SEPT). Animals were implanted intracranially with crystalline OHF or cholesterol, and at the same time received two 10-mm testosterone-filled Silastic capsules SC. Tests for restoration of copulatory behavior were initiated 3 days later, and conducted twice weekly for 2 weeks. Implants of OHF into the MPOA were effective in preventing restoration of male sexual behavior. However, the most effective site was the VMN. Implants of OHF into the AME were only partially effective in stimulating male sexual behavior, whereas implants into the SEPT had no effect. The OHF was discontinued and 1 week later males were retested for sexual behavior. The majority of these animals ejaculated, indicating, that the effects of OHF are reversible. The result of this study demonstrate that the functional integrity of androgen receptors in some, but not all, androgen-concentrating brain loci is necessary for the expression of the complete pattern of male sexual behavior. These data lend support to the view that androgen receptor populations in specific brain loci differentially express proteins involved in mediating the masculine copulatory response.

Amygdala↗
PubMed1985

Alteration of behavioral sex differentiation by exposure to estrogenic compounds during a critical neonatal period: effects of zearalenone, methoxychlor, and estradiol in hamsters.

The present study was designed to determine if neonatal exposure to the estrogenic mycotoxin zearalenone or the weakly estrogenic pesticide methoxychlor could masculinize and/or defeminize the behavior of female hamsters. Neonatal hamsters were given a single sc injection of either zearalenone (1 mg/pup), methoxychlor (1 mg/pup), 17 beta-estradiol (E2) (40 micrograms/pup), or the vehicle 2 days after birth. After puberty, behavioral estrous cyclicity was measured. The females were then ovariectomized, treated with the male hormone testosterone, and tested for their ability to mount a receptive female (a behavior not normally displayed by female hamsters). Females treated neonatally with estradiol or zearalenone were masculinized but not defeminized, an effect consistent with perinatal exposure to low doses of sex hormones. Females in these two treatment groups displayed normal 4-day behavioral estrous cycles, but following ovariectomy and testosterone treatment they mounted a sexually receptive female at a frequency comparable to the males. Methoxychlor-treated females did not differ from controls. The mounting behavior of similarly treated males was unaffected by any of the chemicals. However, males receiving estradiol treatment had smaller testes, seminal vesicles, and cauda epididymides and 57% had epididymal cysts. These results demonstrate that a single exposure to a weakly estrogenic chemical like zearalenone during a critical developmental period can cause the brain to differentiate in a manner inconsistent with the female's genetic sex. This enables the female to respond to the activational influence of testosterone as an adult and readily mount a sexually receptive female. The failure of methoxychlor to alter reproductive development in the current study may be due to an inability of the neonatal hamster to convert methoxychlor to estrogenic metabolites.

Animals↗
PubMed1992

In utero and lactational exposure of male rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin. 2. Effects on sexual behavior and the regulation of luteinizing hormone secretion in adulthood.

When administered to postpubescent male rats, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) decreases plasma androgen concentrations. If such an androgenic deficiency were produced prenatally and/or early postnatally it could impair sexual differentiation of the central nervous system (CNS) and thereby alter male reproductive function. To examine this possibility, sexually dimorphic functions were assessed in male rats born to dams given TCDD (0.064, 0.16, 0.40, and 1.0 micrograms/kg, po) or vehicle on Day 15 of gestation. Masculine sexual behavior was assessed at approximately 60, 75, and 115 days of age. When TCDD-exposed males were caged with receptive control females their mount, intromission, and ejaculation latencies were far longer than normal; these effects were dose-related and were statistically significant at maternal doses as low as 0.16, 0.064, and 0.16 micrograms TCDD/kg, respectively. The numbers of mounts and intromissions to ejaculation were slightly increased by TCDD, while copulatory rates [(mounts+intromissions)/min] were significantly decreased at the three highest maternal doses. Except for a modest increase at the higher doses, TCDD had little effect on the postejaculatory interval. Following assessment of their masculine sexual behavior, the males were castrated and 6 weeks later tested for feminine sexual behavior (lordosis). After being primed with estradiol benzoate and treated with progesterone, males displayed dose-related increases in lordosis quotient and lordosis intensity in response to being mounted by another male. These effects were statistically significant at maternal doses as low as 0.16 and 0.40 micrograms TCDD/kg, respectively. To determine if perinatal TCDD exposure alters the sexually dimorphic regulation of luteinizing hormone (LH) secretion, the LH secretory responsiveness of the hypothalamic/pituitary axis to ovarian steroids was assessed. In unexposed, gonadectomized female rats primed with estradiol benzoate, progesterone injection produced a surge in plasma LH concentrations, whereas in similarly treated control males, plasma LH concentrations were unaffected by progesterone. In castrated, estradiol benzoate-primed male rats that were perinatally exposed to TCDD, progesterone treatment produced dose-related increases in plasma LH concentrations that were statistically significant at the two highest maternal doses. We conclude that in utero and lactational exposure to small amounts of TCDD demasculinizes and feminizes male rats. These effects cannot be accounted for by TCDD-induced hypophagia, modest reductions in adult plasma androgen concentrations, possible nonspecific changes in motor activity, or possible reductions in penile sensitivity to sexual stimulation. The altered sexual behaviors and LH secretion were observed when nearly all TCDD had been excreted (as evidenced by uninduced hepatic ethoxyresorufin-O-deethylase activity).(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗
PubMed1976

Testicular feminization syndrome: current clinical considerations.

The testicular feminization syndrome (TFS) in its complete form results in total feminization due to a nuclear inaction of androgens, and the female role should be supported with postpubertal orchiectomy to avoid the risk of malignancy. Incomplete forms of the syndrome (ITFS) include Type I n which some degree of masculinization may be observed, prompting earlier gonadectomy, and Type II or pseudovaginal perineoscrotal hypospadias (PPSH) which is always characterized by pubertal masculinization, necessitating management and support of these patients as males. Other intersex abnormalities which must be differentiated include true hermaphroditism, the Swyer syndrome, males with 17-ketosteroid reductase deficiency, and Reifenstein's syndrome.

17-Ketosteroids↗
PubMed1990

Neonatal serotonin reduction alters the adult feminine sexual behaviour of golden hamsters.

HPLC analysis of hamster hypothalamic 5HT indicated higher levels in females than in males on day 12 after birth. Levels of 5HT and 5HIAA could be reduced in both sexes by pCPA administration. Male and female hamster pups were treated on days 1-7 or 7-14 after birth with either pCPA, 5HTP or buffer, and tested for feminine and masculine sexual behaviour in adulthood. 5HTP had no effect on behaviour in either sex. pCPA had no effect on masculine sexual behaviour nor did it affect feminine sexual behaviour when given between days 1-7. When administered on days 7-14, pCPA significantly decreased the time that females spent displaying feminine sexual behaviour, while significantly increasing it in males. We, therefore, suggest that serotonin may be modulating a neural substrate already differentiated by androgens.

Aging↗
PubMed1992

Role of monoamines in the male differentiation of the brain induced by androgen aromatization.

Cerebral androgen aromatization has been described as a mechanism responsible for masculinization of the brain, and monoamines seem to be involved in sexual differentiation of the brain. The aim of this study was to investigate the possible implication of monoamines in the masculinization of the brain induced by cerebral androgen aromatization not only in the classic hypothalamic areas but also in some extrahypothalamic ones. For this purpose, 1-day-old male Wistar rats were injected intraventricularly with 5 mg/kg of a suspension of an aromatase inhibitor, LY43578. Saline was administered to male and female control groups. At adulthood, open-field, heterotypical, and homotypical sexual behavior tests were performed and cerebral amines were determined by HPLC-ED. Behavioral tests revealed feminine-like exploratory activity and defecation rate in the treated group, as well as an 89% lordotic response and decreased number of mounts plus intromissions. Testosterone levels were not affected by the treatment. Striatal and limbic serotonergic metabolism showed a sexual dimorphism, higher in males than females, that disappeared in the treated group. From these results, we suggest a possible role of extrahypothalamic serotonin in the mediation of the estrogen-induced mechanisms of behavioral sexual differentiation.

Androgens↗
PubMed1992

Perinatal exposure to morphine affects adult sexual behavior of the male golden hamster.

Duromorph, a long-acting form of morphine, was administered to pregnant golden hamsters and/or their pups over the last 4 days of pregnancy and/or the first 4 days after birth. As adults, offspring were gonadectomized, primed with estrogen and progesterone, and tested for their ability to display feminine sexual behavior when placed with a stud male. They were then given testosterone over a 4-week period and tested for their ability to display masculine sexual behavior in the presence of a receptive female. Perinatal morphine exposure had little effect on the females' ability to display either feminine or masculine sexual behavior. In contrast, feminine sexual behavior was significantly enhanced in males exposed to morphine over the perinatal period. This suggests that exposure to opiates during the critical period of sexual differentiation may prevent the defeminization process in this species.

Animals↗
PubMed1993

Ca2+/calmodulin system: participation on rat sexual hypothalamic differentiation.

Modifications of male rat hypothalamic sexual differentiation after neonatal administration of drugs that participate on the Ca2+/calmodulin system (haloperidol, trifluoperazine, penfluridol, pimozide, and verapamil) were studied. Pups treated 72 h after birth were behaviorally tested on day 120 of extrauterine life. Five tests for homotypical behavior were conducted. Afterwards animals were castrated and tested twice for heterotypical (female) behavior under replacement hormonal therapy. Fifty percent (80% in the case of pimozide) of all treated males showed lordotic behavior compared with none of the controls. Haloperidol (39%, lordosis quotient) and pimozide (40%, lordosis quotient) were more active than the others. Results obtained with verapamil were not statistically different from the controls. Pimozide was the most active agent influencing the appetitive masculine behavior (mount latency, intromission latency, and postejaculatory interval). Verapamil was more efficient than the rest of the drugs on the consummatory behavior (mount latency, intromission frequency, interintromission interval, and ejaculatory latency). Our results support the participation of the Ca2+/calmodulin system in hypothalamic sexual differentiation and in the differential modulation of the masculine and feminine behavioral patterns.

Animals↗
PubMed1987

sdc-1: a link between sex determination and dosage compensation in C. elegans.

Mutations in the X-linked gene sdc-1 affect both sex determination and X-chromosome dosage compensation in C. elegans, providing evidence that these two pathways share a common step. In XX animals (normally hermaphrodites), sdc-1 mutations cause partial masculinization and elevated levels of X-linked gene expression, an apparent shift of both pathways toward their XO modes of expression. The masculinization occurs through effects on the major sex determination pathway, upstream of all previously identified sex-determining genes. XO animals are apparently unaffected by the sdc-1 mutations. We propose a model in which the wild-type sdc-1 activity is either a component of the primary sex-determining signal (the X/Autosome ratio) or involved in transmitting information about this signal to both the sex determination and dosage compensation pathways.

Animals↗