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PubMed1986

Basal and HCG-stimulated testosterone production by interstitial cells of the Mongolian gerbil (Meriones unguiculatus)--II. Influence of glucocorticosteroids and steroidal precursors.

Compared to testosterone production by Mongolian gerbil interstitial cells in the absence of HCG or precursors, testosterone formation was significantly elevated by the addition of 100 ng pregnenolone, progesterone, 17-hydroxyprogesterone or DHEA. Production increased linearly with the amounts of precursors added (pregnenolone: r = 0.99; progesterone: r = 0.98; 17-OH-progesterone: r = 0.96; DHEA: r = 0.92, N = 40, all P less than 0.001). Approximately 50% of DHEA were converted to testosterone during the 6-hr incubation period. Neither the addition of 100 ng 11-deoxycortisol, 11-deoxycorticosterone, cortisol, corticosterone, cortisone, 18-OH-corticosterone, 21-deoxycortisone or 11-dehydrocorticosterone, nor of 100 ng estradiol had a significant effect on testosterone production by isolated interstitial cells incubated without or with 1 mIU HCG. Testosterone production by isolated interstitial cells was significantly increased within 2 min after the addition of 100 ng DHEA; production then linearly increased with the length of incubation (r = 0.98, N = 40, P less than 0.001). After addition of as little as 2 ng DHEA, testosterone formation was higher than by cells incubated without DHEA. While testosterone production could not be stimulated by the addition of 1-500 microIU HCG during a 30-min incubation period, it was drastically elevated by the addition of 10, 20 or 100 ng DHEA. Steroidal precursor concentrations secreted by the Mongolian gerbil adrenal gland incubated in vitro for 120 min were too low to stimulate testosterone production by interstitial cells. On the other hand, testosterone synthesis could be increased by the addition of 10-100-microliter aliquots of adrenal extracts.

17-alpha-Hydroxyprogesterone↗

PubMed1980

The effects of cytochalasin B on testosterone synthesis by interstitial cells of rat testis.

The present study examined the effects of cytochalasin B on various steps in the luteinizing hormone (LH)-stimulated increase in testosterone synthesis by collagenase-dispersed interstitial cells of adult rat testis. Cytochalasin B at a concentration range of 0.1--50 microM inhibited the LH-stimulated increase in testosterone synthesis in a dose-dependent manner. Both intracellular and medium (released) testosterone levels were reduced, thus indicating that the decrease was not due to the accumulation of testosterone inside the cell as a result of cytochalasin B treatment. Cytochalasin B also inhibited the 8-bromocyclic AMP and pregnenolone-stimulated testosterone synthesis in a similar dose-dependent manner. Cytochalasin B at the two higher doses (10 and 50 microM) also inhibited the LH-stimulated generation of cyclic AMP by interstitial cells. However, this drug had no effect on basal testosterone synthesis except at the highest concentration added. Previous studies on adrenocorticotropic hormone (ACTH)- and LH-stimulated increase in glucocorticoid and testosterone synthesis in adrenal and Leydig cells, respectively, demonstrated that cytochalasin B or anti-actin inhibited the transport of cholesterol into mitochondria. The present studies suggest that cytochalasin B inhibits at least two additional steps in the LH-stimulated increase in testosterone synthesis: (1) the generation of cyclic AMP at the level of the plasma membrane, and (2) the conversion of pregnenolone to testosterone at the level of the smooth endoplasmic reticulum. It remains to be established whether these are direct effects of cytochalasin B, or whether they are mediated by disruption of microfilaments by cytochalasin B.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1995

Immobilization-induced stress decreases lipogenesis in sebaceous glands as well as plasma testosterone levels in male Syrian hamsters.

The effects of immobilization-induced stress on plasma testosterone levels and lipogenesis in the sebaceous gland were examined in male Syrian hamsters. To induce immobilization stress, the animals were placed in the prone position and wrapped with flexible steel wire gauze at room temperature. Plasma testosterone levels were determined by radioimmunoassay (RIA) of blood samples and sebaceous lipogenesis was determined by measurement of the incorporation of a lipid precursor, 14C-acetate, in ear skin biopsy samples. Both specimens were obtained immediately after the hamsters were decapitated. Immobilization stress for 4 consecutive days produced a marked fall in plasma testosterone levels and sebaceous lipogenesis. These reductions were reversible, the decreased plasma testosterone levels and decreased sebaceous lipogenesis recovering to the nonstressed or prestimulus levels after approximately 1 week. In 4-day stressed animals in occurrence with a decrease in plasma testosterone, sebaceous lipogenesis in ear with topical application of a small dose of testosterone, which have no effect on plasma testosterone level, was equivalent to that in nonstressed animals. These findings indicated that immobilization-induced stress lowered testosterone secretion, and consequently the testosterone levels in the skin, resulting in decreased lipogenesis in the skin. These results thus suggest that psychological or physiological stress can influence cutaneous function by inducing changes in the neuroendocrine system.

Animals↗

PubMed1992

Effect of serum and serum lipoproteins on testosterone production by adult rat Leydig cells in vitro.

The effect of serum factors other than luteinizing hormone on Leydig cell testosterone secretion was examined using an in vitro bioassay system based on the stimulation of purified adult rat Leydig cells during a 20 h incubation in the presence of a maximal dose of human chorionic gonadotrophin (hCG). Charcoal-extracted serum and testicular interstitial fluid (IF) from normal adult male rats were separated into lipoprotein and lipoprotein-deficient fractions by density ultracentrifugation. Stimulatory bioactivity was found in the lipoprotein fraction of both serum and IF, although the levels of lipoprotein and corresponding bioactivity recovered from IF were significantly lower (25%) than those of serum. There was no difference between the effects of serum lipoproteins on Leydig cell testosterone production stimulated by either hCG or dibutyryl cAMP. In time-course studies, the serum lipoprotein fraction had no effect on hCG-stimulated testosterone production in vitro at 3.0 or 6.0 h, but partially prevented the normal decline in hCG-stimulated testosterone production after 6.0 h. In contrast, unfractionated serum was stimulatory at all time-points. In the absence of hCG, the lipoprotein fraction was stimulatory at both 6.0 and 20 h, although not at 3.0 h. The lipoprotein-deficient protein fraction of serum had no effect on hCG-stimulated testosterone production alone, but significantly enhanced the bioactivity of the lipoprotein fraction, and caused a dose-dependent stimulation of testosterone production in the presence of a constant concentration of serum lipoproteins. Both a stimulatory peak of activity (apparent MW 40-80 kDa), and a large MW (> 100 kDa) inhibitor of testosterone production were identified in serum after fractionation by gel filtration (Sephadex G-100). The data indicate that (i) the stimulatory effect of serum on short-term hCG-stimulated Leydig cell testosterone production in vitro is predominantly due to the serum lipoprotein fraction, possibly by providing additional precursors for testosterone synthesis, (ii) the biological activity of the lipoproteins is influenced by both stimulatory and inhibitory serum proteins in addition to luteinizing hormone, and (iii) that serum lipoproteins may be involved in supporting Leydig cell steroidogenesis in vivo.

Animals↗

PubMed1993

Testosterone regulates mitochondrial aspartate aminotransferase gene expression and mRNA stability in prostate.

The effect of testosterone on the precursor mitochondrial aspartate aminotransferase (pmAAT) gene and on pmAAT-mRNA was studied in rat ventral prostate (VP) and pig prostate epithelial cells. Castration significantly decreased the level of nuclear pmAAT transcripts in VP; whereas testosterone treatment of castrated animals restored the level of pmAAT transcripts. Correspondingly, castration resulted in a marked decrease in the transcription rate of the pmAAT gene; whereas testosterone treatment markedly increased the transcription rate. In vitro studies with isolated pig prostate epithelial cells demonstrated that testosterone directly and rapidly induced a transient increase in the transcription rate of the pmAAT gene. The increase in transcription was associated with an increase in the steady-state level of pmAAT-mRNA. Similar in vitro effects were observed with isolated VP epithelial cells. In addition to its stimulatory effect on transcription of the pmAAT gene, testosterone also increased the half-life of pmAAT-mRNA from 2 h in the absence of hormone to 16 h in its presence. Consequently, testosterone appears to stabilize the pmAAT-mRNA. The combination of its immediate effect on stimulating the transcription of the pmAAT gene and its stabilizing effect on pmAAT-mRNA would account for the increase in the steady-state level of pmAAT-mRNA by testosterone. These studies support our proposal that, through these effects, testosterone increases the biosynthesis of mAAT thereby increasing the transamination of aspartate to oxaloacetate and ultimately increasing the synthesis of citrate. This appears to provide at least one of the mechanisms by which testosterone regulates prostate citrate production.

Animals↗

PubMed2006

Estradiol, testosterone, and the risk for hip fractures in elderly men from the Framingham Study.

BACKGROUND: Low serum estradiol has been more strongly associated with low bone mineral density in elderly men than has testosterone, but its association with incident hip fracture is unknown. We examined whether low estradiol increases the risk for future hip fracture among men and explored whether testosterone levels influence this risk. METHODS: We examined 793 men (mean age = 71 years) evaluated between 1981 and 1983, who had estradiol measures and no history of hip fracture, and followed until the end of 1999. Total estradiol and testosterone were measured between 1981 and 1983. Hip fractures were identified and confirmed through medical records review through the end of 1999. We created 3 groups of men based on estradiol levels and performed a Cox-proportional hazards model to examine the risk for incident hip fracture, adjusted for age, body mass index, height, and smoking status. We performed similar analyses based on testosterone levels, and then based on both estradiol and testosterone levels together. RESULTS: There were 39 men who sustained an atraumatic hip fracture over follow-up. Incidence rates for hip fracture (per 1000 person-years) were 11.0, 3.4, and 3.9 for the low (2.0-18.1 pg/mL [7-67 pmol/L]), middle (18.2-34.2 pg/mL [67-125 pmol/L]), and high (> or =34.3 pg/mL [> or =126 pmol/L]) estradiol groups, respectively. With adjustment for age, body mass index, height, and smoking status, the adjusted hazard ratios for men in the low and middle estradiol groups, relative to the high group, were 3.1 (95% confidence interval [CI], 1.4-6.9) and 0.9 (95% CI, 0.4-2.0), respectively. In similar adjusted analyses evaluating men by their testosterone levels, we found no significant increased risk for hip fracture. However, in analyses in which we grouped men by both estradiol and testosterone levels, we found that men with both low estradiol and low testosterone levels had the greatest risk for hip fracture (adjusted hazard ratio: 6.5, 95% CI, 2.9-14.3). CONCLUSION: Men with low estradiol levels are at an increased risk for future hip fracture. Men with both low estradiol and low testosterone levels seem to be at greatest risk for hip fracture.

Aged↗

PubMed2005

Testosterone immunization blocks the ovulatory process in laying hens without affecting ovarian follicular development.

The role of testosterone in the ovulatory process in hens has been largely neglected. The aim of the present study was to evaluate if testosterone plays an important role on the ovulatory process in laying hens. The effect of active and passive immunization against testosterone on ovarian follicular development and oviposition was studied. Egg laying percentage was evaluated in hens actively immunized against testosterone-BSA (T-AI; n = 6) or BSA (BSA-AI; n = 6). Oviposition was reduced as antibody titer increased in T-AI hens (r = -0.67; P < 0.01). Ovarian structures were assessed in three animals from each group. Follicles reached preovulatory size in both groups, nonetheless, in T-AI hens follicles at different stages of regression indicated that ovulation was blocked by treatment. In the remaining animals, preovulatory concentrations of progesterone and testosterone were determined. A preovulatory surge release of progesterone, preceded by a testosterone peak, was observed in the BSA-AI group (P < 0.05). In contrast, progesterone in T-AI animals remained at basal concentrations. Whereas, testosterone concentrations were significantly greater in T-AI as compared with BSA-AI animals (P < 0.05). Finally, to study the effect of passive immunization on oviposition, hens were passively immunized (PI) on four occasions, on alternate days with anti-T serum (T-PI; n = 10) or anti-BSA serum (BSA-PI; n = 8). During the 13-day period that preceded treatment, oviposition averaged 94.1%. Forty-eight hours after the first immunization, no egg was laid by 8 out of the 10 T-PI hens. During the 10 days following the first passive immunization, there was a reduction in the laying percentage that was significantly greater in T-PI hens (reduction of 52% in T-PI versus 29% in P-BSA, P < 0.01). In summary, these studies show that testosterone immunization hampers egg-laying without affecting ovarian follicular development, suggesting that testosterone has an important role in the ovulatory process in laying hens.

Animals↗

PubMed2005

Effect of testosterone on functional recovery in a castrate male rat stroke model.

Both increased and decreased testosterone levels have been reported to correlate with poor outcome after acute ischemic stroke. The present study focused on the role of testosterone during recovery from neurological deficits in a rat focal ischemia model. Castrate male rats were subjected to behavioral tests after 90 min of middle cerebral artery occlusion (MCAO). On day 7 post-MCAO, neurological deficit-matched rats were assigned to a treatment group implanted with subcutaneous testosterone pellets or a control group implanted with sham cholesterol pellets. After 4 weeks post-MCAO, the average infarct volume was not significantly different between the two groups. Rats in the testosterone group demonstrated significantly earlier improvement in neurological deficits and shortened latency of adhesive tape removal compared with the control group as analyzed by Wilcoxon signed ranks test. Walking on parallel bars improved in both groups with a trend towards early recovery observed in the testosterone group. Biased left body swings persisted during the test period in both groups post-MCAO. Serum testosterone was within physiological levels in the treatment group but was not detectable in the control group by radioimmunoassay. GAP-43 and synaptophysin expression did not differ between groups. Less GFAP expression and reactive astrocyte hypertrophy were found around the infarct area in testosterone-treated rats compared with control rats. In conclusion, testosterone replacement post-MCAO accelerated functional recovery in castrate rats, suggesting a potential therapeutic role for testosterone replacement in stroke recovery.

Androgens↗

PubMedDate not supplied

Low free testosterone is an independent risk factor for Alzheimer's disease.

The purpose of this study was to assess pituitary gonadotropins and free testosterone levels in a larger cohort of men with Alzheimer's disease (AD, n=112) and age-matched controls (n=98) from the Oxford Project to Investigate Memory and Ageing (OPTIMA). We measured gonadotropins (follicle stimulating hormone, FSH, and luteinizing hormone, LH), sex hormone binding globulin (SHBG, which determines the amount of free testosterone) and total testosterone (TT) using enzyme immunoassays. AD cases had significantly higher LH and FSH and lower free testosterone levels. LH, FSH and SHBG all increased with age, while free testosterone decreased. Low free testosterone was an independent predictor for AD. Its variance was overall explained by high SHBG, low TT, high LH, an older age and low body mass index (BMI). In controls, low thyroid stimulating hormone levels were also associated with low free testosterone. Elderly AD cases had raised levels of gonadotropins. This response may be an attempt to normalize low free testosterone levels. In non-demented participants, subclinical hyperthyroid disease (a risk factor for AD) which can result in higher SHBG levels, was associated with low free testosterone. Lowering SHBG and/or screening for subclinical thyroid disease may prevent cognitive decline and/or wasting in men at risk for AD.

Aged↗

PubMed2006

Prostate cancer risk in testosterone-treated men.

Men with classical androgen deficiency have reduced prostate volume and blood prostate-specific antigen (PSA) levels compared with their age peers. As it is plausible that androgen deficiency partially protects against prostate disease, and that restoring androgen exposure increases risk to that of eugonadal men of the same age, men using ART should have age-appropriate surveillance for prostate disease. This should comprise rectal examination and blood PSA measurement at regular intervals (determined by age and family history) according to the recommendations, permanently revisited, published by ISSAM, EAU, Endocrine Society.... Testosterone replacement therapy is now being prescribed more often for aging men, the same population in which prostate cancer incidence increases; it has been suggested that administration in men with unrecognised prostate cancer might promote the development of clinically significant disease. In hypogonadal men who were candidates for testosterone therapy, a 14% incidence of occult cancer was found. A percentage (15.2%) of prostate cancer has been found in the placebo group (with normal DRE and PSA) in the prostate cancer prevention study investigating the chemoprevention potential of finasteride. The hypothesis that high levels of circulating androgens is a risk factor for prostate cancer is supported by the dramatic regression, after castration, of tumour symptoms in men with advanced prostate cancer. However these effects, seen at a very late stage of cancer development, may not be relevant to reflect the effects of variations within a physiological range at an earlier stage. Data from all published prospective studies on circulating level of total and free testosterone do not support the hypothesis that high levels of circulating androgens are associated with an increased risk of prostate cancer. A study on a large prospective cohort of 10,049 men, contributes to the gathering evidence that the long standing "androgen hypothesis" of increasing risk with increasing androgen levels can be rejected, suggesting instead that high levels within the reference range of androgens, estrogens and adrenal androgens decrease aggressive prostate cancer risk. Indeed, high-grade prostate cancer has been associated with low plasma level of testosterone. Furthermore, pre-treatment total testosterone was an independent predictor of extraprostatic disease in patients with localized prostate cancer; as testosterone decreases, patients have an increased likelihood of non-organ confined disease and low serum testosterone levels are associated with positive surgical margins in radical retropubic prostatectomy. A clinical implication of these results concerns androgen supplementation which has become easier to administer with the advent of transdermal preparations (patch or gel) that achieve physiological testosterone serum levels without supra physiological escape levels. During the clinical development of a new testosterone patch in more than 200 primary or secondary hypogonadal patients, no prostate cancer was diagnosed.

Androgens↗

PubMed2005

Modulation of Leishmania donovani infection and cell viability by testosterone in bone marrow-derived macrophages: signaling via surface binding sites.

Androgens can increase susceptibility toward numerous parasitic infections as well as modulate apoptosis of immune cells. According to the current view, androgens mediate immune cell activities not only through classical intracellular androgen receptors (AR), but also through membrane receptors on the cell surface. Here, using murine bone marrow-derived macrophages (BMMs), we examined the influence of testosterone on Leishmania donovani infection and cell viability in vitro as well as the possible mechanisms. Our data demonstrated that testosterone directly increased intramacrophage infection by L. donovani. In addition, testosterone decreased cell viability by way of apoptosis, accompanied by increased Fas, FasL, and Caspase-8 expression. However, these effects of testosterone could not be associated with the classical AR in BMMs since AR was not detectable using different experimental techniques. Instead, it was found that testosterone could bind to the surface of BMMs by the use of an impermeable testosterone-BSA-FITC in confocal laser scanning microscopy and flow cytometry. Collectively, our data indicated that the influence of testosterone on L. donovani infection and viability of BMMs was mediated through the binding sites of testosterone on cell surfaces, which provided a novel mode of direct action of testosterone on AR-free BMMs.

Animals↗

PubMed2005

Altered bioavailability of testosterone in androgen-binding protein-transgenic mice.

Serum and intra-testicular total and free testosterone levels in different age groups of mice (7-360-day-old) were analyzed by radioimmunoassay (RIA) in age-matched wild type (WT)-control and in transgenic mice homozygous to rat androgen-binding protein (ABP-TG), in order to identify possible causes of increased pre-pubertal germ cell apoptosis, spermatogenetic defect and reduced fertility seen in ABP-TG mice. Total intra-testicular testosterone levels in the pre-pubertal ABP-TG (7, 14, 21 and 30-day-old) mice were significantly lower than those in age-matched WT-controls. After puberty (60 days and older) the total intra-testicular testosterone levels were higher than those in age-matched WT-controls and increased gradually, peaking on day 180. Serum total testosterone levels in ABP-TG mice did not differ from those in WT-control until day 30. However, a significant increase in the level of serum total testosterone was observed from day 60. Serum and intra-testicular free testosterone levels were significantly lower in 30, 120, 180 and 360-day-old ABP-TG mice than in age-matched WT-controls. Immunohistochemistry for the cholesterol side-chain cleavage (cytochrome P450) enzyme and quantitative real-time RT-PCR analysis of mRNAs for androgen receptor and for enzymes related to steroidogenesis did not show any changes in 30-day-old ABP-TG mice, indicating that the rates of steroidogenesis and utilization were not altered. Human chorionic gonadotrophin (hCG) administration to adult ABP-TG mice increased the intra-testicular total and free testosterone as well as total germ cell counts. We conclude that the presence of greater than physiological concentration of ABP in the mouse testis alters the ratio of free/bound testosterone, and thereby decreases the availability of free testosterone. As a result, a heightened wave of germ cell apoptosis during the pre-pubertal period followed by a reduction in germ cell numbers and reduced fertility is seen in these mice.

Androgen-Binding Protein↗

PubMed2004

Rapid suppression of testosterone secretion after capture in male American alligators (Alligator mississippiensis).

All reptiles studied to date show an increase in circulating corticosterone following capture. This rise in corticosterone has also been shown in a number of instances to result in a decline in reproductive steroids within hours after capture. As a result of these observations it has been considered imperative to collect blood samples as soon as possible after capture to get reliable measures of reproductive hormones. It has been claimed, however, that there is no effect of capture stress on reproductive steroids in juvenile alligators held for 2 h following capture. As we generally reject blood samples that are not collected within 15 min of capture we decided to reinvestigate the effect of short-term capture (2 h) on corticosterone and testosterone in male alligators. Four groups of alligators, ranging in size from 74 to 212 cm total length were captured in a 2-week period in May, the time of year when testosterone levels are highest. Two groups were captured during the day (eight bled at capture and again at 2 h, eight bled at 2 h only) and two at night (10 bled at capture and again at 2 h, 10 bled at 2 h only). Testosterone and corticosterone in alligators bled immediately on capture and at 2 h were not significantly different in the AM and PM samples so the results were combined (Initial bleed: corticosterone, 0.95 +/- 0.09 ng/ml, n=18; testosterone, 6.06 +/- 2.09 ng/ml, n=18. Two-hour bleed: corticosterone 15.68 +/- 1.91, n=18; testosterone, 2.75 +/- 0.79, n=18). Both the increase in corticosterone and the decline in testosterone at 2 h were significant (p<0.05). Corticosterone and testosterone in the alligators sampled only once at 2 h were not significantly different from the 2-h values in alligators sampled twice (corticosterone 15.04 +/- 1.29, n=18; testosterone, 1.85 +/- 0.62, n=18). These results clearly demonstrate that short-term capture stress results in a significant decline in testosterone in male alligators.

Alligators and Crocodiles↗

PubMed2005

High levels of LH and testosterone in a tropical seabird with an elaborate courtship display.

For birds breeding in temperate areas, territoriality and courtship co-occur during spring and are mirrored by elevated plasma levels of luteinizing hormone (LH) and testosterone. By contrast, several tropical species show no major changes in LH and testosterone throughout the year and plasma levels are often low. This study describes changes in body condition, LH and testosterone levels throughout breeding in a tropical seabird, the magnificent frigatebird (Fregata magnificens). Although bi-parental care is the rule in frigatebirds, these seabirds are unique among seabirds in having a lek-like mating system where males perform an elaborate courtship display during which an extravagant sexual ornament (gular pouch) is inflated. Body condition peaked during the displaying stage in males and declined gradually in both sexes, being the lowest during chick-rearing. LH and testosterone titers were the highest in displaying males with a fully inflated gular pouch (means: 23.6 ng/ml for LH and 6.2 ng/ml for testosterone) and remained low (means: 3.8 ng/ml for LH and 0.3 ng/ml for testosterone) during incubation and chick-rearing in both sexes. Body condition was positively related to testosterone levels in displaying males. In male frigatebirds, high levels of testosterone are not associated with aggression but are probably required to display the inflated gular pouch and to perform an elaborate courtship display. Because males invest in incubation and chick-rearing, testosterone has to return to low levels, to permit parental care. This hormonal pattern differs greatly with that of the few tropical seabirds studied so far and is probably related to the unique reproductive strategy of frigatebirds.

Aggression↗

PubMed2003

Changes in masculine sexual behavior, corticosterone and testosterone in response to acute and chronic stress in male rats.

Chronic exposure to stressors increases HPA axis activity and concomitantly reduces HPG axis activity. This antagonistic relationship between both these axes has been proposed to underlie the inhibition of reproductive function due to stress. Sexual behavior in males may be the most vulnerable aspect of male reproduction to acute and chronic stress and it has been suggested that alterations in sexual behavior during stress are due to the antagonistic relationship between testosterone and corticosteroids. However, only in a few studies has a correlation between the levels of testosterone and corticosterone, and sexual behavior been made. In this study, we evaluated the effects of different stressors, applied both acute and chronically, on masculine sexual behavior and whether or not these effects on sexual behavior are accompanied by changes in plasma levels of corticosterone and testosterone. Additionally, we evaluated the effect of testosterone treatment on the effects of stress on sexual behavior. Sexually experienced male rats were exposed to one of the following stressors: immobilization (IMB), electric foot shocks (EFS) or immersion in cold water (ICW). Sexual behavior and plasma levels of testosterone and corticosterone were assessed on days 1, 5, 10, 15, and 20 of stress. In a second experiment, males were castrated, treated with 3 different doses of testosterone propionate (TP) and exposed to ICW for 20 consecutive days. Sexual behavior was assessed on days 1, 5, 10, 15, and 20 and steroids were evaluated on day 20. Parameters of masculine sexual behavior were modified depending on the characteristics of each stressor. Mount, intromission and ejaculation latencies increased significantly, the number of mounts increased, and ejaculations decreased significantly in males exposed to EFS and to ICW but not in males exposed to IMB. Associated with these effects, testosterone decreased in the EFS and ICW groups on days 1, 15, and 20. However, corticosterone increased only in males exposed to ICW. In castrated males, TP treatment failed to block the effects of stress by ICW on sexual behavior and corticosterone. These results indicate that the effects of stress on sexual behavior depend on the characteristics of each stressor, and these effects, as well as the decrease in testosterone are not necessarily associated with the increase in corticosterone. The fact that testosterone treatment did not prevent the effects of stress on sexual behavior suggests that other mediators could be involved in the alterations of sexual behavior caused by stress.

Acute Disease↗

PubMed2004

Experimentally increased testosterone affects social rank and primary sex ratio in the spotless starling.

It has been suggested that the amount of maternal testosterone allocated into the eggs might be implicated in the process of sex determination. However, recent findings on the effect that female social rank has on the level of egg testosterone suggest that reported associations between male-biased sex ratios and yolk testosterone may represent an indirect hormonal effect mediated by the interdependence among maternal hormones, female social rank, and sex ratio. Here, we report the results of a field experiment in which we manipulated the circulating levels of testosterone in female spotless starlings (Sturnus unicolor) before egg formation. Focal females were controlled in subsequent years to explore possible delayed effects of hormone manipulation on primary sex ratio and social status that could persist because of permanent hormonal change or through hormone-dominance interactions. The results indicate that testosterone-implanted females (T-females) produced significantly more sons than control females (C-females) in the year in which they were manipulated. These differences in offspring sex ratio between T- and C-females persisted in the next 3 years, although no additional hormone treatments were given. These results were not mediated by an eventual effect of testosterone treatment on the quality of the females' mates. A similar proportion of T- and C-females acquired a nest box and bred either in the manipulation year or in Year 1 after manipulation, but T-females tended to be more successful in acquiring a nest box than C-females in Years 2 and 3 after manipulation. These results suggest that added testosterone had a direct role on the acquisition and maintenance of high social rank. Delayed effects of testosterone on primary sex ratio might have been caused by altered endogenous production of T-females. Alternatively, the maintenance of sex ratio differences between T- and C-females long after having being implanted might be attributed to the positive effect that enhanced social rank of T-females has on their circulating testosterone levels.

Analysis of Variance↗

PubMed2006

Testosterone and corticosterone during the breeding cycle of equatorial and European stonechats (Saxicola torquata axillaris and S. t. rubicola).

Northern-temperate male birds show seasonal changes in testosterone concentrations with a peak during the breeding season. Many tropical birds express much lower concentrations of testosterone with slight elevations during breeding. Here we describe testosterone and corticosterone concentrations of male stonechats from equatorial Kenya during different substages of breeding and molt. This tropical species has a short breeding season of approximately 3 months. We compare their hormone concentrations to previously published data of males of a northern-temperate relative, the European stonechat, also a seasonal breeder but with a breeding season of approximately 5 months. Equatorial stonechats show a pronounced peak of testosterone during the nest-building and laying stage. During all other stages, testosterone concentrations are low, similar to other year-round territorial tropical bird species. Corticosterone concentrations peak also during the nest-building and laying stage suggesting that this period of maximum female fecundity is a demanding period for the male. Equatorial stonechats have significantly lower concentrations of testosterone than European stonechats during all stages, except during the nest-building and laying stage. During this stage of maximum female fertility, testosterone levels tend to be higher in equatorial than in European stonechats. Our results suggest that equatorial stonechats belong to a group of tropical bird species that are characterized by a short breeding season and a brief high peak of testosterone during the female's fertile period. Such brief, but substantial peaks of testosterone may be common in tropical birds, but they may easily be missed if the exact breeding stage of individual birds is not known.

Animals↗

PubMed2001

Testosterone modulates the dendritic architecture of arcuate neuroendocrine neurons in adult male rats.

Recent studies have demonstrated that gonadectomy of adult male rats induces dendritic growth of neuroendocrine neurons in the arcuate nucleus. We have hypothesized that these changes are secondary to the loss of testosterone negative feedback. In the present study, we examined the effects of testosterone replacement on the dendritic morphology of arcuate neuroendocrine neurons in castrated rats. Rats were orchidectomized and implanted with silastic capsules designed to produce physiological levels of plasma testosterone (n=9) or empty silastic capsules (n=9) for 2 months. Retrograde labeling with systemically injected Fluoro-Gold, followed by intracellular injection of labeled neurons in a fixed slice preparation, were used to visualize arcuate neuroendocrine neurons. Quantitative analysis of dendritic morphology was performed using three-dimensional computer reconstruction. Serum levels of LH (luteinizing hormone) and testosterone were measured by radioimmunoassay. Treatment of castrated rats with physiological levels of testosterone significantly reduced dendritic length, volume and terminal branch number relative to the castrated rats receiving empty silastic capsules. Dendritic spine density was also greater in the testosterone-treated animals, although the total numbers of spines per dendrite was not significantly different between the two groups. In addition, testosterone replacement was effective in reducing serum LH to levels found in intact rats. These studies demonstrate that testosterone replacement suppresses the dendritic outgrowth of arcuate neuroendocrine neurons that occurs in response to castration. The parallel changes in dendritic arbor and serum LH after castration and hormone replacement suggests that the suppressive effects of testosterone are related to steroid negative feedback.

Animals↗