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Abstract Researchers have long sought to understand and predict an animal’s response to stressful stimuli. Since the introduction of the concept of homeostasis, a variety of model frameworks have been proposed to describe what is necessary for an animal to remain within this stable physiological state and the ramifications of leaving it. Romero et al. (Horm Behav 55(3):375–389, 2009) introduced the reactive scope model to provide a novel conceptual framework for the stress response that assumes an animal’s ability to tolerate a stressful stimulus may degrade over time in response to the stimulus. We provide a mathematical formulation for the reactive scope model using a system of ordinary differential equations and show that this model is capable of recreating existing experimental data. We also provide an experimental method that may be used to verify the model as well as several potential additions to the model. If future experimentation provides the necessary data to estimate the model’s parameters, the model presented here may be used to make quantitative predictions about physiological mediator levels during a stress response and predict the onset of homeostatic overload. 

Abstract To further elucidate the role that wear‐and‐tear plays in the transition from acute to chronic stress, we manipulated the intensity and duration of applied chronic stress to determine if behavior would respond proportionately. We brought wild house sparrows into captivity and subjected them to high‐stress, medium‐stress, low‐stress, or captivity‐only. We varied the number of stressors per day and the duration of stress periods to vary wear‐and‐tear, and thus the potential to exhibit chronic stress symptoms. The behaviors we assessed were neophobia (the fear of the new; assessed via food approach latency) and perch hopping (activity). We predicted that our birds would show proportionate decreases in neophobia and activity throughout a long‐term chronic stress paradigm. Our results indicate that neophobia is sensitive to the intensity of chronic stress, however, the birds became more neophobic, which was the opposite of what we expected. Conversely, perch hopping did not differ across treatment groups and is thus not sensitive to the intensity of chronic stress. Together, these data show that different behavioral measurements are impacted differently by chronic stress. 

Abstract The reactive scope model was created to address two major unanswered questions in stress physiology: how and when does the adaptive acute stress response turn into harmful chronic stress? Previous studies suggest that immunoenhancement should occur in reactive homeostasis (acute stress) and immunosuppression should occur in homeostatic overload (chronic stress). We used this dichotomy of immune function to further elucidate the transition from acute to chronic stress by treating house sparrows (Passer domesticus) with different intensities of chronic stress and then monitoring their immune function. By varying the number of stressors given per day and the length of chronic stress bouts over a period of 6 months, we produced four treatment groups: high, medium, and low stress, and captivity‐only. We tracked immunity through the bacterial killing assay and monitored healing of a 4 mm skin biopsy punch. We hypothesized that higher‐stress birds would repair their skin more slowly and have lower bacterial killing capacity. The opposite was true—high‐stress birds initially repaired their skin fastest. Additionally, all birds dramatically reduced bacterial killing capacity after the biopsy and increased food‐derived uric acid, suggesting increased energy acquisition and a shift in immune resources to a more immediate concern (healing). Once healing finished, only the high‐stress birds were unable to recover circulating immune function, suggesting that the combination of high stress and an immune challenge pushed these birds into homeostatic overload. Prioritizing healing over other immunological processes might be the best defense for a bird in its natural habitat. 

The acute stress response can be considered the primary evolutionary adaptation to maximise fitness in the face of unpredictable environmental challenges. However, the difficulties of assessing physiology in natural environments mean comparatively little is known about how response variation influences fitness in free-living animals. Currently, determining acute stress physiology typically involves blood sampling or cardiac monitoring. Both require trapping and handling, interrupting natural behaviour, and potentially biasing our understanding toward trappable species/individuals. Importantly, limits on repeated sampling also restrict response phenotype characterisation, vital for linking stress with fitness. Surface temperature dynamics resulting from peripheral vasomotor activity during acute stress are increasingly promoted as alternative physiological stress indicators, which can be measured non-invasively using infrared thermal imaging, overcoming many limitations of current methods. Nonetheless, which aspects of stress physiology they represent remains unclear, as the underlying mechanisms are unknown. To date, validations have primarily targeted the hypothalamic-pituitary-adrenal axis, when the sympathetic-adrenal-medullary (SAM) system is likely the primary driver of vasomotor activity during acute stress. To address this deficit, we compared eye and bill region surface temperatures – measured using thermal imaging – with SAM system activity – measured as heart-rate-variability via electrocardiogram telemetry – in wild-caught captive house sparrows (Passer domesticus), during capture and handling. We found lower body surface temperatures were associated with increased sympathetic nervous system activation. Consequently, our data confirm body surface temperatures can act as a proxy for sympathetic activation during acute stress, providing potentially transformative opportunities for linking the acute stress response with fitness in the wild. 

Measuring corticosterone in feathers allows researchers to make long-term, retrospective assessments of physiology with non-invasive sampling. To date, there is little evidence that steroids degrade within the feather matrix, however this has yet to be determined from the same sample over many years. In 2009, we made a pool of European starling (Sturnus vulgaris) feathers that had been ground to a homogenous powder using a ball mill and stored on a laboratory bench. Over the past 14 years, a subset of this pooled sample has been assayed via radioimmunoassay (RIA) 19 times to quantify corticosterone. Despite high variability across time (though low variability within assays), there was no effect of time on measured feather corticosterone concentration. In contrast, two enzyme immunoassays (EIA) produced higher concentrations than the samples assayed with RIA, though this difference is likely due to different binding affinities of the antibodies used. The present study provides further support for researchers to use specimens stored long-term and from museums for feather corticosterone quantification, and likely applies to corticosteroid measurements in other keratinized tissues. 

This study highlights innovative, minimally-invasive glucose sensing sutures for monitoring glucose levels in house sparrows. 

One of the biggest unanswered questions in the field of stress physiology is whether variation in chronic stress intensity will produce proportional (a gradient or graded) physiological response. We were specifically interested in the timing of the entrance into homeostatic overload, or the start of chronic stress symptoms. To attempt to fill this knowledge gap we split 40 captive house sparrows (Passer domesticus) into four groups (high stress, medium stress, low stress, and a captivity-only control) and subjected them to six bouts of chronic stress over a 6-month period. We varied the number of stressors/day and the length of each individual bout with the goal of producing groups that would experience different magnitudes of wear-and-tear. To evaluate the impact of chronic stress, at the start and end of each stress bout we measured body weight and three plasma metabolites (glucose, ketones, and uric acid) in both a fasted and fed state. All metrics showed significant differences across treatment groups, with the high stress group most frequently showing the greatest changes. However, the changes did not produce a consistent profile that matched the different chronic stress intensities. We also took samples after a prolonged recovery period of 6 weeks after the chronic stressors ended. The only group difference that persisted after 6 weeks was weight—all differences across groups in metabolites recovered. The results indicate that common blood metabolites are sensitive to stressors and may show signs of wear-and-tear, but are not reliable indicators of the intensity of long-term chronic stress. Furthermore, regulatory mechanisms are robust enough to recover within 6 weeks post-stress. 

Abstract When animals are sick, their physiology and behavior change in ways that can impact their offspring. Research is emerging showing that infection risk alone can also modify the physiology and behavior of healthy animals. If physiological responses to environments with high infection risk take place during reproduction, it is possible that they lead to maternal effects. Understanding whether and how high infection risk triggers maternal effects is important to elucidate how the impacts of infectious agents extend beyond infected individuals and how, in this way, they are even stronger evolutionary forces than already considered. Here, to evaluate the effects of infection risk on maternal responses, we exposed healthy female Japanese quail to either an immune-challenged (lipopolysaccharide [LPS] treated) mate or to a healthy (control) mate. We first assessed how females responded behaviorally to these treatments. Exposure to an immune-challenged or control male was immediately followed by exposure to a healthy male, to determine whether treatment affected paternity allocation. We predicted that females paired with immune-challenged males would avoid and show aggression towards those males, and that paternity would be skewed towards the healthy male. After mating, we collected eggs over a 5-day period. As an additional control, we collected eggs from immune-challenged females mated to healthy males. We tested eggs for fertilization status, embryo sex ratio, as well as albumen corticosterone, lysozyme activity, and ovotransferrin, and yolk antioxidant capacity. We predicted that immune-challenged females would show the strongest changes in the egg and embryo metrics, and that females exposed to immune-challenged males would show intermediate responses. Contrary to our predictions, we found no avoidance of immune-challenged males and no differences in terms of paternity allocation. Immune-challenged females laid fewer eggs, with an almost bimodal distribution of sex ratio for embryos. In this group, albumen ovotransferrin was the lowest, and yolk antioxidant capacity decreased over time, while it increased in the other treatments. No differences in albumen lysozyme were found. Both females that were immune-challenged and those exposed to immune-challenged males deposited progressively more corticosterone in their eggs over time, a pattern opposed to that shown by females exposed to control males. Our results suggest that egg-laying Japanese quail may be able to respond to infection risk, but that additional or prolonged sickness symptoms may be needed for more extensive maternal responses. 

ABSTRACT There are complex interactions between an organism's microbiome and its response to stressors, often referred to as the ‘gut–brain axis’; however, the ecological relevance of this axis in wild animals remains poorly understood. Here, we used a chronic mild stress protocol to induce stress in wild-caught house sparrows (Passer domesticus), and compared microbial communities among stressed animals, those recovering from stress, captive controls (unstressed) and a group not brought into captivity. We assessed changes in microbial communities and abundance of shed microbes by culturing cloacal samples on multiple media to select for aerobic and anaerobic bacteria and fungi. We complemented this with cultivation-independent 16S and ITS rRNA gene amplification and sequencing, pairing these results with host physiological and immune metrics, including body mass change, relative spleen mass and plasma corticosterone concentrations. We found significant effects of stress and captivity on the house sparrow microbiomes, with stress leading to an increased relative abundance of endotoxin-producing bacteria – a possible mechanism for the hyperinflammatory response observed in captive avians. While we found evidence that the microbiome community partially recovers after stress cessation, animals may lose key taxa, and the abundance of endotoxin-producing bacteria persists. Our results suggest an overall link between chronic stress, host immune system and the microbiome, with the loss of potentially beneficial taxa (e.g. lactic acid bacteria), and an increase in endotoxin-producing bacteria due to stress and captivity. Ultimately, consideration of the host's microbiome may be useful when evaluating the impact of stressors on individual and population health.