Testosterone (T) and cortisol (C) are the end products of neuroendocrine axes that interact with the process of shaping brain structure and function. Relative levels of T:C (TC ratio) may alter prefrontal–amygdala functional connectivity in adulthood. What remains unclear is whether TC-related effects are rooted to childhood and adolescence. We used a healthy cohort of 4–22-year-olds to test for associations between TC ratios, brain structure (amygdala volume, cortical thickness (CTh), and their coordinated growth), as well as cognitive and behavioral development. We found greater TC ratios to be associated with the growth of specific brain structures: 1) parietal CTh; 2) covariance of the amygdala with CTh in visual and somatosensory areas. These brain parameters were in turn associated with lower verbal/executive function and higher spatial working memory. In sum, individual TC profiles may confer a particular brain phenotype and set of cognitive strengths and vulnerabilities, prior to adulthood.

Background: It has been suggested that hypercortisolism contributes to the pathophysiology of Alzheimer's disease (AD), based on the fact that excess glucocorticoid exposure has potent adverse effects on the central nervous system. In contrast, dehydroepiandrosterone (DHEA) has been linked to a broad range of beneficial physiological effects including neuronal excitability and neuroprotection and even memory enhancing properties. Of note, proinflammatory cytokines are present in neuritic plaques (a hallmark of AD) and may regulate cortisol/DHEA release. In this exploratory study, we hypothesized that there is a flattened diurnal curve of cortisol and DHEA in mild to moderate AD, linked to increased cytokine levels.

Methods: Diurnal profiles of cortisol, adrenocorticotropic hormone (ACTH), and DHEA were studied in 15 patients with mild to moderate AD (7 men and 8 women, 75.6 ± 5.5 years) and 15 healthy elderly controls (7 men and 8 women, 73.3 ± 5.8 years, respectively). Interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and soluble TNF receptors were analyzed.

Results: Women with AD had significantly increased morning levels of ACTH, DHEA, and IL-6 compared to healthy elderly women. Cortisol levels were significantly increased in men with AD at 0300 h versus healthy elderly men, in spite of slightly decreased ACTH levels.

Conclusions: Our data suggest important sex differences in hypothalamic–pituitary–adrenal (HPA) axis regulation and steroid hormone clearance in patients with AD. Increased secretion of IL-6 may have a contributory role in this difference.

Several lines of indirect evidence suggest that subjects with latent infection of the coccidian parasite Toxoplasma gondii have a higher concentration of testosterone than uninfected controls. Here, we searched for direct evidence of latent toxoplasmosis-associated differences in testosterone concentration among a population of 174 female and 91 male students screened for Toxoplasma infection. We have found Toxoplasma-infected men to have a higher concentration of testosterone and Toxoplasma-infected women to have a lower concentration of testosterone than Toxoplasma-free controls. The opposite direction of the testosterone shift in men compared to women can explain the observed gender specificity of behavioural shifts in Toxoplasma-infected subjects.

This study was conducted to verify the effect(s) of melatonin treatment on frog Leydig cells. Morphological observation after melatonin treatment indicates that many frog Leydig cells show degenerative changes (i.e. heterochromatic nuclei, loss of cellular adhesion) while in adjacent germinal tubules several Sertoli cells show heterochromatic nuclei, confirming the presence of a paracrine effect between interstitial and germinal compartments. The effect of melatonin on frog Leydig cell steroidogenesis was investigated in in vitro experiments; after 6 h of incubation melatonin severely inhibits both control and GnRH-induced testosterone secretion. In addition, in order to verify the effect of indolamine on frog Leydig cell activity, we investigated, by in situ hybridization, the presence of frog relaxin (fRLX, a transcript specifically expressed by these cells) in the testes of melatonin-injected animals after 48 h. fRLX signal completely disappeared from the testis of melatonin-injected frogs. The results of the present study indicate that melatonin treatment provokes Leydig cell morphological changes, blocks GnRH-antagonist-induced testosterone secretion and decreases fRLX expression. Taken together these results strongly indicate that melatonin acts on Leydig cells in the testis of the frog Rana esculenta.

Historically, studies of the role of endogenous hormones in developmental differentiation of the sexes have suggested that mammalian sexual differentiation is mediated primarily by testicular androgens, and that exposure to androgens in early life leads to a male brain as defined by neuroanatomy and behavior. The female brain has been assumed to develop via a hormonal default mechanism, in the absence of androgen or other hormones. Ovarian hormones have significant effects on the development of a sexually dimorphic cortical structure, the corpus callosum, which is larger in male than in female rats. In the females, removal of the ovaries as late as Day 16 increases the cross-sectional area of the adult corpus callosum. Treatment with low-dose estradiol starting on Day 25 inhibits this effect. Female callosa are also enlarged by a combination of daily postnatal handling and exogenous testosterone administered prior to Day 8. The effects of androgen treatment are expressed early in development, with males and testosterone-treated females having larger callosa than control females as early as Day 30. The effects of ovariectomy do not appear until after Day 55. These findings are more consistent with other evidence of a later sensitive period for ovarian feminization as compared to androgenic masculinization.

Forty-eight Greyface wether lambs, aged about 6 months and weighing 32 kg on average were used. They were allocated to be treated, by subcutaneous implantation in the upper surface of the ear flap, with the naturally occurring steroids oestradiol-17β (O), testosterone (T) or the synthetically produced androgen trenbolone acetate (TA). Treatment groups were as follows: sham-implanted controls (C); 50 mg O (slow release formulation) (O); 40 mg TA (compressed pellets} (TA); 50 mg T (compressed pellets) (T); 15 mg O + 40 mg TA (TAO); 15 mg O + 50 mg T (TO). Combined implants were placed in close proximity under the skin of the same ear. The lambs were offered, to appetite, a good quality diet containing per kg dry matter (DM) an estimated 12-0 MJ metabolizable energy and 150 g crude protein. Comparisons were made for the main effects of O and the androgens T and TA. Main effects due to O were increased DM intake, live-weight gain (LWG) empty body weight (EBW), chilled carcass iveight (CCW), carcass crude protein (CP) deposition, plasma insulin concentrations and teat length with reductions recorded for the proportion but not weight of fat in the carcass, plasma urea and thyroxine concentrations. Treatment with androgens did not, on average, influence LWG or other indices of growth performance or carcass composition other than to produce significant increases in carcass phosphorus deposition and reduction in the depth of thorax. Significant increases in the iveight of penile tissue and reductions in teat length were recorded. There was evidence for a greater androgenic effect on penile tissue and anti-oestrogenic effect (on teat length) of TA compared with T at the concentrations used. TA also reduced the weight of the thymus gland, an effect reversed in the presence ofO.

Analysis of plasma taken from the vein contralateral to the site of implantation showed that O concentrations were reduced in the presence of TA and T, and that O had no effect on the concentrations of androgens measured. Concentrations ofT and 17 β-hydroxy-trenbolone in blood were of a similar order, which for T is typical of postpubertal entire male sheep.

The results suggest that O treatment was effective in promoting growth and carcass CP deposition which was not increased by T or TA, despite the presence of these androgens at biologically active concentrations in blood. This effect appears to differ from the additive effects frequently obtained for castrated male cattle.

Twenty-five Border Leicester ♂ × Blackface ♀ wether lambs aged about 4 months and weighing on average 28·5 kg were allocated to be treated with the naturally occurring steroid testosterone or trenbolone acetate or nandrolone phenylpropionate which are steroids synthetically produced. Treatment groups were as follows: untreated controls (C); 50 mg testosterone (T); 50 mg trenbolone acetate (TA); 50 mg testosterone + 50 mg trenbolone acetate (TTA) or 50 mg nandrolone phenylpropionate (N). Implants were given at 100 and again at 63 days before slaughter. The lambs were offered to appetite a good quality diet containing, per kg dry matter, an estimated 11·0 MJ metabolizable energy and 185 g crude protein. Comparisons were made for the main effects of T and TA and also interactions between T and TA. Effects due to N were assessed statistically against untreated controls. Treatment with T, on average, increased live-weight gain (LWG), empty body weight (EBW) and reduced backfat thickness and the weight (g/kg EBW) of perirenal and retroperitoneal fat. Main effects due to TA were increases in killing-out ratio and depth of the gigot joint and reductions in backfat thickness. Treatment with N increased the empty body weight and (g/kg) carcass ash. Non-significant (P > 0·05) trends were suggested for increases in carcass crude protein due to T and TA treatments. T and TA but not N treatments exhibited marked androgenic activity in increasing the weight (mg/kg EBW) of the accessary vesicular gland. TA and N, but not T, reduced the weight (g/kg EBW) of the thymus gland.

The maximum binding capacity of post-morte m skeletal muscle (m. gluteus) for (3H)-dexamethasone was reduced by TA but increased by T and N. These results suggest differences in the binding capacity of corticosteroid receptors which may be related to differences in the effects of T and TA on protein metabolism in skeletal muscle.