The hypothalamic-pituitary-adrenal (HPA) axis, a neuroendocrine network that controls hormonal responses to internal and external challenges in an organism's environment, exhibits strikingly sex-biased activity. In adult female rodents, acute HPA function following a stressor is markedly greater than it is in males, and this difference has largely been attributed to modulation by the gonadal hormones testosterone and estradiol. These gonadal hormones are produced by the hypothalamic-pituitary-gonadal (HPG) axis and have been shown to determine sex differences in adult HPA function after acute stress via their activational and organizational effects. Although these actions of gonadal hormones are well supported, the possibility that sex chromosomes similarly influence HPA activity is unexplored. Moreover, questions remain regarding sex differences in the activity of the HPA axis following chronic stress and the underlying contributions of gonadal hormones and sex chromosomes. The present review examines what is currently known about sex differences in the neuroendocrine response to stress, as well as outstanding questions regarding this sex bias. Although it primarily focuses on the rodent literature, a brief discussion of sex differences in the human HPA axis is also included.

(1) Tolerance to ad libitum feeding was compared in three genotypes of broiler breeder hens: a standard broiler breeder fed ad libitum (SA) or restricted (SR), a slow growing 'label' broiler breeder (L) and an experimental dwarf heavy broiler breeder (E). Two similar experiments were conducted in two distinct research centres. (2) Feed intake and body weight were measured every 3 weeks from hatch to 40 to 49 weeks of age. Egg production and egg abnormalities were recorded. The number of yellow follicles in ovaries was counted at the age of 32 weeks. (3) Body weight was stabilised at 2.2, 3.7 and 5.4 kg after 24 weeks of age in L, E and SA hens, respectively. Growth of the SR hens was similar to that of L up to 20 weeks and stabilised at a similar level to that of E hens after 30 weeks of age. (4) Sexual maturity was delayed by 6 weeks in restricted breeders compared to ad libitum fed hens that started to lay at 20 weeks. SA hens had low egg production and a high proportion of defective eggs, which was largely compensated for by feed restriction. However, productivity of SR hens remained lower than that of L breeders. (5) Compared to the low viability and reproductive fitness observed with SA hens, the E dwarf broiler breeder tolerated ad libitum feeding and had better egg production, fewer egg abnormalities and yellow follicles per ovary and a higher egg production. However, laying rate was still lower than that of the SR and L groups. Energy conversion (kJ/g egg) from 32 to 40 weeks of age was much higher in the SA group than in the other three groups. 6. The feasibility of feeding a dwarf broiler breeder ad libitum calls for further research on implications of specific IGF and GH-receptor expression at the level of the ovary in dw chickens.

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Estradiol and testosterone are powerful steroid hormones that impact brain function in numerous ways. During development, these hormones can act to program the adult brain in a male or female direction. During adulthood, gonadal steroid hormones can activate or inhibit brain regions to modulate adult functions. Sex differences in behavioral and neuroendocrine (i.e., hypothalamic pituitary adrenal (HPA) axis) responses to stress arise as a result of these organizational and activational actions. The sex differences that are present in the HPA and behavioral responses to stress are particularly important considering their role in maintaining homeostasis. Furthermore, dysregulation of these systems can underlie the sex biases in risk for complex, stress-related diseases that are found in humans. Although many studies have explored the role of estrogen and estrogen receptors in mediating sex differences in stress-related behaviors and HPA function, much less consideration has been given to the role of androgens. While circulating androgens can act by binding and activating androgen receptors, they can also act by metabolism to estrogenic molecules to impact estrogen signaling in the brain and periphery. This review focuses on androgens as an important hormone for modulating the HPA axis and behaviors throughout life and for setting up sex differences in key stress regulatory systems that could impact risk for disease in adulthood. In particular, impacts of androgens on neuropeptide systems known to play key roles in HPA and behavioral responses to stress (corticotropin-releasing factor, vasopressin, and oxytocin) are discussed. A greater knowledge of androgen action in the brain is key to understanding the neurobiology of stress in both sexes.

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