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Article (refereed) -postprintDeviche, Pierre; Gao, Sisi; Davies, Scott; Sharp, Peter J.; Dawson, Alistair. 2012Rapid stress-induced inhibition of plasma testosterone in free-ranging male rufouswinged sparrows, Peucaea carpalis: characterization, time course, and recovery. Endocrinology, 177 (1). 1-8. 10.1016/j.ygcen.2012.02.022 Contact CEH NORA team at noraceh@ceh.ac.uk General and ComparativeThe NERC and CEH trademarks and logos ('the Trademarks') are registered trademarks of NERC in the UK and other countries, and may not be used without the prior written consent of the Trademark owner. 1Rapid stress-induced inhibition of plasma testosterone in free- 25Chronic stress generally inhibits the activity of the reproductive system. Acute stress also is 26 often inhibitory, but the mechanism involved and its persistence of action once animals are no 27 longer exposed to the stressor are poorly understood. We investigated the effect of capture and 28 restraint stress on plasma testosterone (T), luteinizing hormone (LH), and corticosterone 29(CORT) in free-ranging male rufous-winged sparrows, Peucaea carpalis. Stress decreased 30 plasma T between 10 and 30 min after capture and restraint but did not influence plasma LH, 31the main hormone that controls T secretion, suggesting that stress did not decrease plasma T 32 by inhibiting LH secretion. The stress-induced decrease in plasma T was associated with 33 elevated plasma CORT, but there was no evidence that these effects were functionally related. 34Plasma stress-induced T was positively related to plasma initial T measured within 2 min of 35 capture. This relationship was, however, complex as plasma T decreased proportionally more in 36 response to stress in sparrows with high than low plasma initial T. The relative sensitivity to a 37 same stressor was, therefore, individually variable and this variation was related to initial plasma 38 T. Birds caught and restrained for 30 min, and then released on their breeding territory before 39 recapture up to 6 hours later, maintained depressed plasma T, indicating that the effect of acute 40 stress on this hormone persists after the stressor removal. These studies provide new 41 information on the effects of acute stress on plasma T in free-ranging birds. In particular, they decrease plasma T by impairing LH secretion or attenuating the testicular sensitivity to this 77 hormone [13]. Acute stress in birds typically increases plasma CORT in 5-10 min [44,33,69,13] 78 and in the rufous-winged sparrow, plasma T decreases by 30% -50% after capture and 89No study has, to our knowledge, investigated the time course of endocrine recovery from 90 mild acute stress in wild, free-ranging birds. The second objective of the present work was to 106during the study period were in breeding condition [36,12,57]. 108 Capture and blood sample collection 110Sparrows were captured in response to simulated territorial intrusion (STI: conspecific 111 song playback), while they were on their breeding territory and using a Japanese mist ...

We sought to clarify functional relationships between baseline and acute stress-induced changes in plasma levels of the stress hormone corticosterone (CORT) and the reproductive hormone testosterone (T), and those of two main metabolites, uric acid (UA) and glucose (GLU). Acute stress in vertebrates generally stimulates the secretion of glucocorticoids, which in birds is primarily CORT. This stimulation is thought to promote behavioral and metabolic changes, including increased glycemia. However, limited information in free-ranging birds supports the view that acutely elevated plasma CORT stimulates glycemia. Acute stress also often decreases the secretion of reproductive hormones (e.g., T in males), but the role of CORT in this decrease and the contribution of T to the regulation of plasma GLU remain poorly understood. We measured initial (pre-stress) and acute stress-induced plasma CORT and T as well as GLU in adult male Rufous-winged Sparrows, Peucaea carpalis, sampled during the pre-breeding, breeding, post-breeding molt, and non-breeding stages. Stress increased plasma CORT and the magnitude of this increase did not differ across life history stages. The stress-induced elevation of plasma CORT was consistently associated with decreased plasma UA, suggesting a role for CORT in the regulation of plasma UA during stress. During stress plasma GLU either increased (pre-breeding), did not change (breeding), or decreased (molt and non-breeding), and plasma T either decreased (pre-breeding and breeding) or did not change (molt and non-breeding). These data provide only partial support to the hypothesis that CORT secretion during acute stress exerts a hyperglycemic action or is responsible for the observed decrease in plasma T taking place at certain life history stages. They also do not support the hypothesis that rapid changes in plasma T influence glycemia.

Stress-induced effects on innate immune activity in wild birds have been difficult to predict. These difficulties may arise from the frequent assumptions that (1) the stress response influences different components of the immune response similarly, (2) stress-induced effects do not change over the course of the stress response and (3) glucocorticoids are the primary regulators of stress-induced changes of immune activity. We tested the first two assumptions by measuring three components of innate immunity at two times during the stress response in captive adult male house sparrows, Passer domesticus. Acute stress resulting from handling and restraint suppressed plasma lytic and microbicidal activity within 10 min and reduced plasma agglutination ability within 120 min. We tested the third assumption by measuring stress-induced effects in sparrows that were pharmacologically adrenalectomized by mitotane administration. Confirming the effectiveness of this treatment, mitotane-treated birds had lower pre-stress plasma CORT than control birds and showed no increase in plasma CORT during acute stress. The innate immune activity of mitotane-treated birds did not decrease during the stress response, but the pre-stress immune activity of these birds did not differ from that of vehicle-treated birds. These results suggest that elevated plasma CORT during stress is primarily responsible for mediating stress-induced suppression of innate immune activity.

To maximize fitness, organisms must invest energetic and nutritional resources into developing, activating, and maintaining reproductive physiology and behavior. Corticosterone (CORT), the primary avian glucocorticoid, regulates energetic reserves to meet metabolic demands. At low (baseline) plasma levels, CORT activates avian mineralocorticoid receptors and may stimulate lipid mobilization, foraging activity, and feeding behavior. During stress in birds, elevated plasma CORT also stimulates glucocorticoid receptors and may promote glycemia, lipolysis, and proteolysis. Furthermore, CORT orchestrates physiological and behavioral adjustments to perceived threats. While many avian studies demonstrate effects of CORT on reproduction, few studies have elucidated the mechanisms, including receptor activation and site(s) of action, which underlie these effects. Even fewer studies have investigated how low and elevated plasma CORT regulates energetic reserves to meet the metabolic demands of reproduction. Here, we propose several hypotheses to clarify the direct and indirect effects of CORT on avian reproductive physiology and behavior. In addition, we emphasize the need for new manipulative studies involving alterations of endogenous plasma CORT levels and/or food availability to elucidate how CORT regulates the energetic demands of reproduction.