scholarly journals The lingering impact of stress: brief acute glucocorticoid exposure has sustained, dose-dependent effects on reproduction

2018 ◽  
Vol 285 (1882) ◽  
pp. 20180722 ◽  
Author(s):  
Maren N. Vitousek ◽  
Conor C. Taff ◽  
Daniel R. Ardia ◽  
Jocelyn M. Stedman ◽  
Cedric Zimmer ◽  
...  

Acutely stressful experiences can have profound and persistent effects on phenotype. Across taxa, individuals differ remarkably in their susceptibility to stress. However, the mechanistic causes of enduring stress effects, and of individual differences in stress susceptibility, are poorly understood. Here, we tested whether brief, acute increases in glucocorticoid hormones have persistent effects on phenotype, and whether effects differ according to the magnitude or duration of elevation. We used a novel method to non-invasively manipulate hormone levels on short time scales: the application of corticosterone gel to a model egg secured in the nest. Free-living female tree swallows ( Tachycineta bicolor ) exposed to several brief corticosterone increases during incubation showed dose-dependent differences in behaviour throughout the reproductive period. Birds receiving treatments that simulated higher or longer acute stress responses later provisioned larger broods at lower rates; the resulting offspring were smaller in size. Treatment did not influence female body condition, oxidative stress, reproductive success or inter-annual survival, but exposed females maintained higher baseline corticosterone after treatments ceased. Overall, these results indicate that brief, acute elevations in glucocorticoids in adulthood can have long-term consequences. Furthermore, individuals that mount a greater or longer acute stress response may be more likely to experience lingering effects of stress.

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e1590 ◽  
Author(s):  
Matthias Nemeth ◽  
Elisabeth Pschernig ◽  
Bernard Wallner ◽  
Eva Millesi

Non-invasive measurements of glucocorticoid (GC) concentrations, including cortisol and corticosterone, serve as reliable indicators of adrenocortical activities and physiological stress loads in a variety of species. As an alternative to invasive analyses based on plasma, GC concentrations in saliva still represent single-point-of-time measurements, suitable for studying short-term or acute stress responses, whereas fecal GC metabolites (FGMs) reflect overall stress loads and stress responses after a species-specific time frame in the long-term. In our study species, the domestic guinea pig, GC measurements are commonly used to indicate stress responses to different environmental conditions, but the biological relevance of non-invasive measurements is widely unknown. We therefore established an experimental protocol based on the animals’ natural stress responses to different environmental conditions and compared GC levels in plasma, saliva, and fecal samples during non-stressful social isolations and stressful two-hour social confrontations with unfamiliar individuals. Plasma and saliva cortisol concentrations were significantly increased directly after the social confrontations, and plasma and saliva cortisol levels were strongly correlated. This demonstrates a high biological relevance of GC measurements in saliva. FGM levels measured 20 h afterwards, representing the reported mean gut passage time based on physiological validations, revealed that the overall stress load was not affected by the confrontations, but also no relations to plasma cortisol levels were detected. We therefore measured FGMs in two-hour intervals for 24 h after another social confrontation and detected significantly increased levels after four to twelve hours, reaching peak concentrations already after six hours. Our findings confirm that non-invasive GC measurements in guinea pigs are highly biologically relevant in indicating physiological stress responses compared to circulating levels in plasma in the short- and long-term. Our approach also underlines the importance of detailed investigations on how to use and interpret non-invasive measurements, including the determination of appropriate time points for sample collections.


2009 ◽  
Vol 106 (1) ◽  
pp. 66-72 ◽  
Author(s):  
Jonathan E. Campbell ◽  
Nasimeh Rakhshani ◽  
Sergiu Fediuc ◽  
Silvio Bruni ◽  
Michael C. Riddell

Although exercise is a common and potent activator of the hypothalamic-pituitary adrenal (HPA) axis, the effects of exercise on the acute stress response are not well understood. Here, we investigated the effects of short- (2 wk) and long-term (8 wk) voluntary wheel running on adrenal sensitivity to ACTH stimulation and the acute stress response to restraint in male rats. Diurnal glucocorticoid patterns were measured on days 7 (all groups) and 35 (8-wk groups). Rats were subjected to 20 min of restraint stress on either week 1 or on week 7 of treatment to assess HPA activation. One week later, exogenous ACTH (75 ng/kg) was administered to assess adrenal sensitivity to ACTH. Following this, adrenals were collected and analyzed for key proteins involved in corticosterone (CORT) synthesis. By the end of week 1, exercising (E) animals had twofold higher peak diurnal CORT levels compared with sedentary (S) animals ( P < 0.01). CORT values were not different between groups at week 8. In response to restraint stress at week 2, CORT values in E were approximately threefold greater than in S ( P < 0.05). No difference was found between E and S rats in the response to, or recovery from, restraint at week 8. During the ACTH challenge at week 2, E demonstrated a ∼2.5-fold increase in adrenal sensitivity compared with S, while no difference was found between E and S at week 8. The expression of steroidogenic acute regulatory protein was found to be ∼50% higher in the adrenals in E compared with S at week 2 ( P < 0.05), but no difference existed between groups at week 8. These results show that volitional wheel running initially causes hyperactivation of the HPA axis, due to enhanced adrenal sensitivity to ACTH, but that these alterations in HPA activity are completely restored by 8 wk of training.


2020 ◽  
Vol 27 (4) ◽  
pp. 132-153 ◽  
Author(s):  
André Schulz ◽  
Dana Schultchen ◽  
Claus Vögele

Abstract. The brain and peripheral bodily organs continuously exchange information. Exemplary, interoception refers to the processing and perception of ascending information from the body to the brain. Stress responses involve a neurobehavioral cascade, which includes the activation of peripheral organs via neural and endocrine pathways and can thus be seen as an example for descending information on the brain-body axis. Hence, the interaction of interoception and stress represents bi-directional communication on the brain-body axis. The main hypothesis underlying this review is that the dysregulation of brain-body communication represents an important mechanism for the generation of physical symptoms in stress-related disorders. The aims of this review are, therefore, (1) to summarize current knowledge on acute stress effects on different stages of interoceptive signal processing, (2) to discuss possible patterns of abnormal brain-body communication (i.e., alterations in interoception and physiological stress axes activation) in mental disorders and chronic physical conditions, and (3) to consider possible approaches to modify interoception. Due to the regulatory feedback loops underlying brain-body communication, the modification of interoceptive processes (ascending signals) may, in turn, affect physiological stress axes activity (descending signals), and, ultimately, also physical symptoms.


Author(s):  
Eric S. Wohleb

Stress is experienced when stimuli pose a perceived or actual threat to an organism. Exposure to a stressor initiates physiological and behavioral responses that are aimed at restoring homeostasis. In particular, stress activates the hypothalamic-pituitary-adrenal axis, leading to release of glucocorticoids, and engages the autonomic nervous system, causing release of norepinephrine. These “stress hormones” have widespread effects, because most cells express respective receptors that initiate cell-type-specific molecular signaling pathways. In the brain, acute stress promotes neuronal activation, resulting in alertness and adaptive behavioral responses. However, chronic or uncontrolled stress exposure can have deleterious effects on neuronal function, including loss of synaptic connections, which leads to behavioral and cognitive impairments. Stress responses also influence the function of brain-resident microglia and peripheral immune cells that interact with the brain, and alterations in these neuroimmune systems can contribute to the neurobiological and behavioral effects of chronic stress. Ongoing research is aimed at uncovering the molecular and cellular mechanisms that mediate stress effects on neuroimmune systems, and vice versa.


2012 ◽  
Vol 18 (4) ◽  
pp. 678-688 ◽  
Author(s):  
Ildikó Rácz ◽  
Astrid Markert ◽  
Daniela Mauer ◽  
Birgit Stoffel-Wagner ◽  
Andreas Zimmer

2017 ◽  
Vol 27 ◽  
pp. S718
Author(s):  
M. Bloomfield ◽  
R. McCutcheon ◽  
T. Dahoun ◽  
M. Kempton ◽  
L. Valmaggia ◽  
...  

2004 ◽  
Vol 32 (3) ◽  
pp. 627-648 ◽  
Author(s):  
MO Huising ◽  
C van Schooten ◽  
AJ Taverne-Thiele ◽  
T Hermsen ◽  
BM Verburg-van Kemenade ◽  
...  

We elucidated the structure of the principle factors regulating the initiation of the acute stress response in common carp: corticotrophin-releasing hormone (CRH), CRH-receptor 1 (CRH-R1) and CRH-binding protein (CRH-BP). Phylogenetic analyses reveal that these proteins are evolutionarily well conserved in vertebrates. CRH and CRH-BP expression are not co-localised in the same hypothalamic perikarya. On the contrary, CRH-BP expression is limited to the perimeter of the nucleus preopticus (NPO), but is abundant in other regions, including an area directly rostral from, and in close proximity to, the NPO. Despite the lack of co-expression, the nerve fibres projecting onto both the rostral pars distalis (rPD) as well as the large fibre bundles projecting onto the pars intermedia (PI) contain CRH as well as CRH-BP, suggesting that both ACTH release from the rPD as well as the release of PI melanotrope content is regulated via CRH and CRH-BP. Finally, we show via real-time quantitative PCR that expression of hypothalamic CRH and CRH-BP following a 24 h restraint significantly increases, whereas PD CRH-R1 expression decreases; this reflects desensitisation of the PD for hypothalamic CRH output. We conclude that these factors are actively involved in the regulation of acute stress responses in the teleost fish.


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