栖息地的快速城市化改变了自然环境,化学,听觉,人类和野生动物居民的光环境。最普遍的转变之一是由夜间人造光(ALAN)引起的,但尚不清楚个人在多大程度上适应如此迅速的环境变化。这里,我们检验了城市鸟类对有害行为的抵抗力增强的假设,寄生虫学,和阿兰的生理效应。我们捕获了家雀(墨西哥的Haemorhous),一种通常栖息在城市及其自然环境中的鸟,来自凤凰城的两个城市和两个农村,亚利桑那,美国,城市化程度和阿兰强度的多个数量级都不同,并将它们放置在普通的花园实验室环境中。我们在主观夜晚将每种栖息地类型的一半鸟类暴露于生态相关的夜间照明水平,虽然ALAN暴露减少了城市和农村鸟类的睡眠,暴露于ALAN的城市鸟类比暴露于ALAN的农村鸟类睡眠时间更长。我们还发现,ALAN暴露会增加肠球虫寄生虫(Isosporaspp。)在城市和农村的鸟类中,但是相对于农村鸟类,城市鸟类的扩散率较低。我们发现夜间照明抑制了农村而不是城市鸟类的羽毛皮质酮滴度,表明光通过慢性应激或抑制其昼夜节律来损害HPA的功能,城市鸟类再次抵抗这种影响。中介分析表明,在农村鸟类中,ALAN暴露的作用是对羽毛皮质酮的显着睡眠介导的,而不是球虫病。暗示了艾伦改变生理学的多种机制。我们提供了进一步的证据,表明来自夜光栖息地的动物可以对ALAN及其有害影响产生抵抗力。
Rapid urbanization of habitats alters the physical, chemical, auditory, and photic environments of human and wild animal inhabitants. One of the most widespread transformations is caused by artificial light at night (ALAN), but it is not clear the extent to which individuals acclimate to such rapid environmental change. Here, we tested the hypothesis that urban birds show increased resistance to harmful behavioral, parasitological, and physiological effects of ALAN. We captured house
finches (Haemorhous mexicanus), a bird that commonly inhabits cities and their natural surroundings, from two urban and two rural sites in Phoenix, Arizona, USA, which differ by both degree of urbanization and by multiple orders of magnitude in ALAN intensity, and placed them in a common garden laboratory setting. We exposed half of the birds from each habitat type to ecologically relevant levels of night lighting during the subjective night and found that, while ALAN exposure reduced sleep in both urban and rural birds, ALAN-exposed urban birds were able to sleep longer than ALAN-exposed rural birds. We also found that ALAN exposure increased the proliferation rate of an intestinal coccidian parasite (Isospora spp.) in both urban and rural birds, but that the rate of proliferation was lower in urban relative to rural birds. We found that night lighting suppressed titers of feather corticosterone in rural but not urban birds, suggesting that light impairs HPA function through chronic stress or suppression of its circadian rhythmicity, and that urban birds were again resistant to this effect. Mediation analyses show that the effect of ALAN exposure in rural birds was significantly sleep-mediated for feather corticosterone but not coccidiosis, suggesting a diversity of mechanisms by which ALAN alters physiology. We contribute further evidence that animals from night-lit habitats can develop resistance to ALAN and its detrimental effects.