Glucocorticoids (corticosterone in birds and rodents and cortisol in all other mammals) are glucoregulatory hormones that are synthesized in response to a range of stimuli including stress and are regularly measured in the assessment of animal welfare. Glucocorticoids have many normal or non-stress-related functions, and glucocorticoid synthesis can increase in response to pleasure, excitement, and arousal as well as fear, anxiety, and pain. Often, when assessing animal welfare, little consideration is given to normal non-stress-related glucocorticoid functions or the complex mechanisms that regulate the effects of glucocorticoids on physiology. In addition, it is rarely acknowledged that increased glucocorticoid synthesis can indicate positive welfare states or that a stress response can increase fitness and improve the welfare of an animal. In this paper, we review how and when glucocorticoid synthesis increases, the actions mediated through type I and type II glucocorticoid receptors, the importance of corticosteroid-binding globulin, the role of 11 β-hydroxysteroid dehydrogenase, and the key aspects of neurophysiology relevant to activating the hypothalamo-pituitary-adrenal axis. This is discussed in the context of animal welfare assessment, particularly under the biological functioning and affective states frameworks. We contend that extending the assessment of animal welfare to key brain regions afferent to the hypothalamus and incorporating the aspects of glucocorticoid physiology that affect change in target tissue will advance animal welfare science and inspire more comprehensive assessment of the welfare of animals.

There is considerable interest in the potential for measuring cortisol in hair as a means of quantifying stress responses in human and non-human animals. This review updates the rapid advancement in our knowledge of hair cortisol, methods for its measurement, its relationship to acute and chronic stress, and its repeatability and heritability. The advantages of measuring cortisol in hair compared with other matrices such as blood, saliva and excreta and the current theories of the mechanisms of cortisol incorporation into the fibre are described. Hair cortisol as a measure of the physiological response to stress in a variety of species is presented, including correlations with other sample matrices, the relationship between hair cortisol and psychosocial stress and the repeatability and heritability of hair cortisol concentrations. Current standards for the quantification of hair cortisol are critically reviewed in detail for the first time and gaps in technical validation of these methods highlighted. The known effects of a variety of sources of hair cortisol variation are also reviewed, including hair sampling site, sex, age and adiposity. There is currently insufficient evidence to conclude that cortisol concentration in hair accurately reflects long-term blood cortisol concentrations. Similarly, there is a lack of information surrounding the mechanisms of cortisol incorporation into the hair. This review highlights several directions for future research to more fully validate the use of hair cortisol as an indicator of chronic stress.

Hatching success of leatherback turtles, Dermochelys coriacea, is typically ~50%, but the reasons for embryonic death are unknown. We investigated the distribution of egg failure within 16 developing nests to determine whether spatial position or respiratory environment was associated with embryonic death. We measured oxygen and carbon dioxide partial pressures during incubation to investigate whether any spatial variation in developmental success was associated with regions of hypoxia or hypercapnia. Eggs in the centre of nests had a significantly lower mean hatching success (42.1 ± 7.6%) than eggs in the intermediate (66.1 ± 5.3%) and peripheral (69.8 ± 3.5%) regions. Of those eggs that died, there were no significant differences in the timing of early- and late-stage embryonic death in central (77.6 ± 7.2% early death, 17.3 ± 8.2% late death) and peripheral (80.8 ± 10.1% early death, 14.7 ± 5.8% late death) regions. Oxygen tension in all regions of nests was significantly lower and carbon dioxide tension was significantly higher than in control nests by Day 35 of incubation. Although spatial variation in respiratory gases was detected, it did not appear to explain spatially variable developmental success because late-stage embryonic death did not increase in the central region where oxygen tension was lowest and carbon dioxide tension was highest.

This review focuses on the importance of cortisol in mediating the inhibitory effects of psychosocial stress on reproduction in females. In particular, we have summarized our research in sheep where we have systematically established whether cortisol is both sufficient and necessary to suppress reproductive hormone secretion and inhibit sexual behaviour. Our findings are put into context with previous work and are used to develop important concepts as well as to identify productive further lines of investigation. It is clear that cortisol is necessary to inhibit some, but not all, aspects of reproduction in female sheep. These actions vary with reproductive state, and there are important interactions with gonadal steroids. The impact of cortisol on the tonic secretion of gonadotrophin-releasing hormone and luteinizing hormone has been investigated extensively, but less is known about the surge secretion of these hormones and their effects on sexual behaviour. Furthermore, there are separate effects of cortisol in the brain (hypothalamus) and at the anterior pituitary, illustrating that there are different mechanisms of action. Thus, although cortisol is important in mediating some of the effects of stress on reproduction, we need to look beyond cortisol and investigate some of the other mechanisms and mediators that relay the effects of stress on reproduction. In this regard, we propose that a group of neurons in the hypothalamus that co-synthesize kisspeptin, neurokinin B and dynorphin, termed KNDy cells, play important roles in mediating the effects of cortisol on reproduction. This hypothesis needs to be rigorously tested.Reproduction (2016) 152 R1-R14