Many host species have evolved sophisticated defences to mitigate the high fitness costs imposed by brood parasitism. Even though the physiological mechanisms behind such defences can offer important insights into the evolutionary relationship between brood parasites and hosts, they have received little attention so far. Hormones play a critical role in the regulation of bird reproduction, which make them a key element when investigating the physiological effects of brood parasitism on hosts. Here, we experimentally parasitized Eurasian blackbird (Turdus merula) nests with non-mimetic eggs to study its impact on the hormonal levels (corticosterone and prolactin) of females during incubation, as well as the magnitude of the response to the standardized stress protocol in parasitized and non-parasitized individuals. Parasitized females had higher baseline corticosterone levels and showed a poorer body condition than non-parasitized birds, while we found no differences for prolactin levels. Both parasitized and non-parasitized females responded to the standardized-stress protocol with a significant increase in corticosterone levels. However, the decrease in prolactin after the standardized stress protocol was significantly more pronounced in parasitized individuals. Our results suggest that the presence of a non-mimetic parasitic egg involves a stressful situation for hosts, negatively affecting the physical state of parasitized females. Unaffected prolactin levels of parasitized individuals could explain the absence of nest desertion found in this species in response to parasitism. Finally, both hormones were not correlated in blackbirds, confirming that their combined study provides valuable pieces of information on the endocrine mechanisms underlying behavioural responses in animals, including hosts of brood parasites. Significance statementPhysiological mechanisms behind avian brood parasitism remain unclear. In this study, we assessed the effect of experimental parasitism on the hormonal profiles of hosts. We found that the presence of a non-mimetic egg in the nest modified baseline corticosterone levels, but not prolactin levels, of parasitized females and negatively impacted their body condition. Moreover, experimental parasitism affected the prolactin response to stress. These results expand previous information on the endocrine consequences of brood parasitism at other stages of the breeding cycle (nestling and fledgling stage) and might shed light on the hormonal mechanisms that underlie the host response against parasitic eggs. Communicated by M. Leonard
BackgroundTraditional theory assumes that egg recognition and rejection abilities arise as a response against interspecific brood parasitism (IBP). However, rejection also appears in some species that are currently not exploited by interspecific parasites, such as Turdus thrushes. Recent evidences suggest that rejection abilities evolved in these species as a response to conspecific brood parasitism (CBP). To test these two alternative hypotheses, we performed an experimental study by parasitizing nests of the common blackbird (Turdus merula) with conspecifics or heterospecific eggs under different risk of parasitism (presence of interspecific or conspecific parasites near the nest). Common blackbird is a potential host of the common cuckoo (Cuculus canorus) but suffers low levels of CBP too.ResultsWe found that blackbirds were able to recognize and eject heterospecific eggs at high rates whereas most of conspecifics eggs were not recognized and, therefore, accepted. Ejection rates of conspecific eggs did not exceed 13 %, even in situations of high risk of CBP (blackbird female placed near the nest), which contradict the main prediction derived from the CBP hypothesis. Conversely, ejection rates of experimental eggs simulating IBP were much higher (80–100 %). Furthermore, female blackbirds were more aggressive towards cuckoos than towards blackbird dummies.ConclusionsOur results considered together support the IBP hypothesis, indicating that recognition and rejection of parasitic eggs in blackbirds have probably evolved due to previous cuckoo parasitism. The current absence of IBP in blackbirds may be due to the highly efficient rejection abilities in this species. Thus, these abilities have been retained in absence of brood parasitism as a consequence of the low costs involved for blackbirds, resulting in a successful resistance against interspecific brood parasitism.
Prolonged social isolation has negative effects on brain and behavior in humans and other social organisms, but neural mechanisms leading to these effects are not understood. Here we tested the hypothesis that even brief periods of social isolation can alter gene expression and DNA methylation in higher cognitive centers of the brain, focusing on the auditory/associative forebrain of the highly social zebra finch. Using RNA sequencing, we first identified genes that individually increase or decrease expression after isolation and observed general repression of gene sets annotated for neurotrophin pathways and axonal guidance functions. We then pursued 4 genes of large effect size: EGR1 and BDNF (decreased by isolation) and FKBP5 and UTS2B (increased). By in situ hybridization, each gene responded in different cell subsets, arguing against a single cellular mechanism. To test whether effects were specific to the social component of the isolation experience, we compared gene expression in birds isolated either alone or with a single familiar partner. Partner inclusion ameliorated the effect of solo isolation on EGR1 and BDNF, but not on FKBP5 and UTS2B nor on circulating corticosterone. By bisulfite sequencing analysis of auditory forebrain DNA, isolation caused changes in methylation of a subset of differentially expressed genes, including BDNF. Thus, social isolation has rapid consequences on gene activity in a higher integrative center of the brain, triggering epigenetic mechanisms that may influence processing of ongoing experience.
Traffic is often acknowledged as a threat to biodiversity, but its effects have been mostly studied on roads subjected to high traffic intensity. The impact of lower traffic intensity such as those affecting protected areas is generally neglected, but conservation-oriented activities entailing motorized traffic could paradoxically transform suitable habitats into ecological traps. Here we questioned whether roadside-nesting bee-eaters Merops apiaster perceived low traffic intensity as a stressor eliciting risk-avoidance behaviors (alarm calls and flock flushes) and reducing parental care. Comparisons were established within Doñana National Park (Spain), between birds exposed to either negligible traffic (ca. 0–10 vehicles per day) or low traffic intensity (ca. 10–90 vehicles per day) associated to management and research activities. The frequencies of alarm calls and flock flushes were greater in areas of higher traffic intensity, which resulted in direct mortality at moderate vehicle speeds (≤ 40 km/h). Parental feeding rates paralleled changes in traffic intensity, but contrary to our predictions. Indeed, feeding rates were highest in traffic-exposed nests, during working days and traffic rush-hours. Traffic-avoidance responses were systematic and likely involved costs (energy expenditure and mortality), but vehicle transit positively influenced the reproductive performance of bee-eaters through an increase of nestling feeding rates. Because the expected outcome of traffic on individual performance can be opposed when responses are monitored during mating (i.e. negative effect by increase of alarm calls and flock flushes) or nestling-feeding period (i.e. at least short-term positive effect by increase of nestling feeding rates), caution should be taken before inferring fitness consequences only from isolated behaviors or specific life history stages.
Obligate avian brood parasites lay their eggs in the nest of other bird species, known as hosts. Brood parasitism often imposes severe fitness costs on hosts, selecting for the evolution of effective antiparasitic defences, such as recognition and rejection of brood parasite eggs. Glucocorticoids have been recently found to mediate host physiological and behavioral adjustments in response to brood parasite eggs; however, it remains unclear whether brood parasitism triggers a general response involving multiple physiological elements. In this study, we experimentally investigated whether a salient brood parasitic stimulus (the presence of a nonmimetic model egg in the nest) causes physiological adjustments in adult Eurasian blackbirds (Turdus merula) at immune (leukocyte profiles) and cellular (heatshock protein Hsp70 synthesis) level. Also, we explored whether these physiological changes are mediated by variations in corticosterone (CORT) levels. We found that experimental brood parasitism caused an increase in heterophils and a decrease in lymphocytes, leading to higher heterophils and lymphocytes ratios in parasitized birds. Nevertheless, we did not find tradeoffs between immune function and CORT levels. Hsp70 synthesis was not affected by our experimental manipulation. Our findings provide evidence that brood parasite eggs trigger a general stress response in egg-rejecter hosts, including changes in cellular immune profiles.
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