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The ability for traits to recover after exposure to stress varies depending on the magnitude, duration, or type of stressor. One such stressor is circadian rhythm disruption stemming from exposure to light at night. Circadian rhythm disruption may lead to long-term physiological consequences; however, the capacity in which individuals recover and display stress resilience is not known. Here, we exposed zebra finches (Taeniopygia castanotis) to constant light (24L:0D) or a regular light/dark cycle (14L:10D) for 23 days, followed by a recovery period for 12 days. We measured body mass, corticosterone, and glucose levels at multiple timepoints, and relative protein expression of glucocorticoid receptors at euthanasia. Body mass significantly increased over time in light-exposed birds compared to controls, but a 12-day recovery period reversed this increase. Baseline levels of circulating glucose decreased in light-exposed birds compared to controls, but returned to pretreatment levels after the 12-day recovery period. In contrast, the glucose stress response did not show a similar recovery trend, suggesting longer recovery is needed or that this is a persistent effect in light-exposed birds. Surprisingly, we did not detect any differences in baseline corticosterone or reactivity of the hypothalamic-pituitiary-adrenal (HPA) axis between groups throughout the experiment. Moreover, we did not detect differences between relative protein expression of glucocorticoid receptors or a relationship with HPA axis reactivity. Yet, we found a positive relationship between glucocorticoid receptors and the glucose stress response, but only in the light group. Our results indicate that physiological and morphological traits differ in their ability to recover in response to constant light and warrants further investigation on the mechanisms driving stress resilience under a disrupted circadian rhythm. 

ABSTRACT Many songbirds begin active incubation after laying their penultimate egg, resulting in synchronous hatching of the clutch except for a last‐hatched individual (“runt”) that hatches with a size deficit and competitive disadvantage to siblings when begging for food. However, climate change may elevate temperatures and cause environmental incubation as eggs are laid, resulting in asynchronous hatching and larger size hierarchies among siblings. Although previous work demonstrated that asynchronous hatching reduces nestling growth and survival relative to synchrony, the physiological mechanisms underlying these effects are unclear. To test the effects of asynchronous hatching on runt growth, survival, physiology, and compensatory growth‐related tradeoffs, we manipulated incubation temperature in nest boxes of European starlings (Sturnus vulgaris) to increase asynchronous hatching and collected nestling morphological measurements and blood samples to assess physiology and development. Independent of heating treatment, runts from asynchronously hatched nests had lower survival than runts from more synchronous nests. Surviving runts from asynchronous nests were smaller and had reduced stress‐induced corticosterone concentrations and reduced circulating glucose compared with runts from synchronous nests. Despite persistent size and energy deficits, runts from asynchronous nests did not have significant deficits in immunity or telomere length when compared with runts from synchronous nests, suggesting no trade‐off between investment in immune development or telomere maintenance with growth. Overall, these results suggest that increased asynchrony due to climate change could reduce clutch survival for altricial songbirds, especially for the smallest chicks in a clutch, and that the negative effects of asynchrony may be driven by persistent energetic deficits. 

Avoidance of novel stimuli (neophobia) affects how wild animals interact with their environment and may partly determine whether animals persist in human-altered landscapes. The neuroendocrine mediators of neophobia are poorly understood, although past work demonstrated that experimentally reducing circulating corticosterone in wild-caught house sparrows (Passer domesticus) decreased neophobia toward novel objects placed near the food dish. In this experiment, we directly tested the role of one of the two types of corticosterone receptors, the glucocorticoid receptor (GR), in mediating neophobia in house sparrows by administering a GR antagonist (RU486, n = 10) or a vehicle control (peanut oil, n = 10) over 5 consecutive days and measuring responses to novel objects both pre- and post-treatment. We also measured baseline and stress-induced corticosterone in all sparrows on the final day of behavior trials. To better understand the effects of RU486 on corticosterone over time, in a separate group of sparrows (n = 12) we administered RU486 or vehicle over 5 days and took multiple blood samples to assess baseline and stress-induced corticosterone. Overall, we did not detect an effect of subcutaneous RU486 injections on neophobia behavior. However, we did find that RU486 injections significantly decreased stress-induced corticosterone levels starting 1 day post-injection and baseline corticosterone levels starting 6 days post-injection, compared to vehicle-injected controls. Our results suggest that GR is not involved in mediating neophobia behavior in house sparrows. 

Some individuals respond to new objects, foods, or environments with wariness (neophobia), whereas others are willing to approach and explore. Because novel stimuli can represent both dangers and resources, group-living species may show adaptive plasticity in neophobia in response to social cues. To better understand how conspecific calls can influence neophobia in a highly gregarious species, we exposed individual house sparrows (Passer domesticus) to either conspecific alarm calls (n = 12), conspecific contact calls (n = 12), or no playback (n = 12) and measured latency to feed in the presence of novel objects. We also measured novelty responses with no sound the week before and after the sound treatment week for all individuals. Relative to no playback and contact calls, we predicted that conspecific alarm calls would increase neophobia behavior during the acoustic trial and that these effects would persist the week after exposure. Instead, we found that individuals in the contact call and no playback groups became less neophobic as weeks progressed, while the alarm call group showed no attenuation of neophobia. There was a significant interaction between week and treatment, where neophobia responses over the three weeks were significantly different for individuals exposed to alarm calls compared to the contact and no playback groups combined. These results suggest that house sparrows learn social information about potentially threatening stimuli from conspecific alarm calls; here, that novel objects may be dangerous. 

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.