The secretion of glucocorticoids (GCs) is a classic endocrine response to stress. Despite that, it remains controversial as to what purpose GCs serve at such times. One view, stretching back to the time of Hans Selye, posits that GCs help mediate the ongoing or pending stress response, either via basal levels of GCs permitting other facets of the stress response to emerge efficaciously, and/or by stress levels of GCs actively stimulating the stress response. In contrast, a revisionist viewpoint posits that GCs suppress the stress response, preventing it from being pathologically overactivated. In this review, we consider recent findings regarding GC action and, based on them, generate criteria for determining whether a particular GC action permits, stimulates, or suppresses an ongoing stressresponse or, as an additional category, is preparative for a subsequent stressor. We apply these GC actions to the realms of cardiovascular function, fluid volume and hemorrhage, immunity and inflammation, metabolism, neurobiology, and reproductive physiology. We find that GC actions fall into markedly different categories, depending on the physiological endpoint in question, with evidence for mediating effects in some cases, and suppressive or preparative in others. We then attempt to assimilate these heterogeneous GC actions into a physiological whole. (Endocrine Reviews 21: 55‐ 89, 2000)

/pdf/how-do-glucocorticoids-influence-stress-responses-4egr3fa2k0.pdf

How do glucocorticoids influence stress responses? Integrating permissive, suppressive, stimulatory, and preparative actions.

The concept of allostasis in biology and biomedicine.

SYNOPSIS. Superimposed upon seasonal changes in morphology, physiology and behavior, are facultative responses to unpredictable events known as labile ( i.e. , short-lived) perturbation factors (LPFs). These responses include behavioral and physiological changes that enhance survival and collectively make up the “emergency” life history stage. There is considerable evidence that glucocorticosteroids, and other hormones in the hypothalamo—pituitary—adrenal (HPA) cascade, initiate and orchestrate the emergency life history stage within minutes to hours. This stage has a number of sub—stages that promote survival and avoid potential deleterious effects of stress that may result from chronically elevated levels of circulating glucocorticosteroids over days and weeks. These sub—stages may include: redirection of behavior from a normal life history stage to increased foraging, irruptivetype migration during the day, enhanced restfulness at night, and elevated gluconeogenesis. Once the perturbation passes, glucocorticosteroids may also promote recovery. Additional evidence from birds indicates that glucocorticosteroid responses to a standardized capture, handling and restraint protocol are modulated both on seasonal and individual levels. Field work reveals that these changes in responsiveness to LPFs have ecological bases, such as reproductive state, body condition etc., that in turn indicate different hormonal control mechanisms in the HPA cascade.

/pdf/ecological-bases-of-hormone-behavior-interactions-the-51sxihwmf0.pdf

Ecological bases of hormone-behavior interactions : the emergency life history stage

Environmental and social stresses have deleterious effects on reproductive function in vertebrates. Global climate change, human disturbance and endocrine disruption from pollutants are increasingly likely to pose additional stresses that could have a major impact on human society. Nonetheless, some populations of vertebrates (from fish to mammals) are able to temporarily resist environmental and social stresses, and breed successfully. A classical trade-off of reproductive success for potential survival is involved. We define five examples. (i) Aged individuals with minimal future reproductive success that should attempt to breed despite potential acute stressors. (ii) Seasonal breeders when time for actual breeding is so short that acute stress should be resisted in favour of reproductive success. (iii) If both members of a breeding pair provide parental care, then loss of a mate should be compensated for by the remaining individual. (iv) Semelparous species in which there is only one breeding period followed by programmed death. (v) Species where, because of the transience of dominance status in a social group, individuals may only have a short window of opportunity for mating. We suggest four mechanisms underlying resistance of the gonadal axis to stress. (i) Blockade at the central nervous system level, i.e. an individual no longer perceives the perturbation as stressful. (ii) Blockade at the level of the hypothalamic-pituitary-adrenal axis (i.e. failure to increase secretion of glucocorticosteroids). (iii) Blockade at the level of the hypothalamic-pituitary-gonad axis (i.e. resistance of the reproductive system to the actions of glucocorticosteroids). (iv) Compensatory stimulation of the gonadal axis to counteract inhibitory glucocorticosteroid actions. Although these mechanisms are likely genetically determined, their expression may depend upon a complex interaction with environmental factors. Future research will provide valuable information on the biology of stress and how organisms cope. Such mechanisms would be particularly insightful as the spectre of global change continues to unfold.

Reproduction and resistance to stress: When and how

Seasonal changes in plasma glucocorticoid concentrations in free-living vertebrates.

Modulation of the adrenocortical response to stress in birds

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Modulation of the adrenocortical response to stress in birds