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The primary objectives of this paper are to define, explore the environmental factors favoring, and discuss hypotheses concerning the endocrine bases of two important arctic breeding strategies that we call spatial and temporal opportunism. We identify several species that display spatial opportunism in the Arctic, and one that displays temporal opportunism. In spatial opportunism, breeding may be highly seasonal but the locality where individuals breed may change from year to year as a result of unpredictable spatial distribution of food, nest site availability, or other factors such as predator abundance. We suggest that flexibility of the transition from migration to settlement distinguishes spatial opportunists from site-faithful migrants. Thus far, data are available for only two hypotheses regarding the endocrine basis of this flexibility. Circulating patterns of testosterone (associated with territory establishment) and corticosterone (associated with migratory activity) appear not to be involved in the regulation of spatial opportunism in white-crowned sparrows (Zonotrichia leucophrys gambelii), but more detailed study is necessary. In temporal opportunism (that may occur simultaneously with spatial opportunism), temporally variable food availability apparently selects for the capacity to initiate reproduction across a wide portion of the year. Tonic activity of the hypothalamo-pituitary-gonad (HPG) axis could provide a mechanism to minimize the delay between discovery of abundant food and onset of nesting in any season. However, the evidence for one arctic temporal opportunist, the white-winged crossbill (Loxia leucoptera), indicates that the HPG axis is not tonically active, but probably switches off (i.e., becomes photorefractory) in autumn, as for other birds breeding at these latitudes. Opportunistic breeding very early in the year (e.g., March near Fairbanks, Alaska) is associated with increased luteinizing hormone secretion, probably in response to a combination of abundant food and social stimuli, after refractoriness dissipates. We have taken the first step of identifying spatial and temporal opportunism as important phenomena in the Arctic, and discussing hypotheses related to endocrine mechanisms. Future research should identify specific environmental cues involved, and elucidate the neuroendocrine and endocrine mechanisms underlying these two reproductive strategies.

Stress-induced inhibition of innate immune activity is widespread in free-ranging birds, but the mechanisms that are responsible for this inhibition are poorly understood. We previously demonstrated that an increase in plasma corticosterone (CORT), the primary avian glucocorticoid, is necessary for the inhibition of natural antibody- and complement-mediated as well as bactericidal activities to occur during stress. Here we investigated the role of glucocorticoid receptors in stress-induced inhibition of natural antibody- and complement-mediated activities and bactericidal activity within non-genomic (<10 min) and genomic (<120 min) time frames in male House Sparrows, Passer domesticus . Treatment with the selective glucocorticoid receptor antagonist mifepristone (RU486) attenuated stress-induced suppression of natural antibody-mediated activity within 10 min and 120 min of experimental stress. By contrast, this treatment did not influence stress-induced suppression of complement-mediated or bactericidal activity. These results suggest that stress-induced elevated plasma CORT inhibits natural antibody-mediated activity, but not complement-mediated or bactericidal activity, by activating glucocorticoid receptors, and that both non-genomic and genomic mechanisms underlie this activation. Additional research is needed to identify the receptors that regulate inhibitory effects of elevated plasma CORT on complement-mediated and bactericidal activity. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Since the discovery of gonadotropin-releasing hormone (GnRH) in mammals at the beginning of the 1970s, it was generally accepted that GnRH is the only hypothalamic neuropeptide regulating gonadotropin release in mammals and other vertebrates. In 2000, however, gonadotropin-inhibitory hormone (GnIH), a novel hypothalamic neuropeptide that actively inhibits gonadotropin release, was discovered in quail. Numerous studies over the past decade and a half have demonstrated that GnIH serves as a key player regulating reproduction across vertebrates, acting on the brain and pituitary to modulate reproductive physiology and behavior. In the latter case, recent evidence indicates that GnIH can regulate reproductive behavior through changes in neurosteroid, such as neuroestrogen, biosynthesis in the brain. This review summarizes the discovery of GnIH, and the contributions to GnIH research focused on its mode of action, regulation of biosynthesis, and how these findings advance our understanding of reproductive neuroendocrinology. [ABSTRACT FROM AUTHOR]

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., (© 2017. Published by The Company of Biologists Ltd.)