Hormonal responses to non-mimetic eggs: is brood parasitism a physiological stressor during incubation?

Abstract

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

Host defences against avian brood parasitism: an endocrine perspective

“…Furthermore, hormones may underlie variation in host defences at the within-individual ( plasticity), betweenindividual and across-species levels, potentially facilitating evolution of plastic defences to fixed responses [19]. A small number of studies have begun to uncover the hormonal responses of avian hosts to brood parasites at the within-species [20][21][22][23] and across-species levels [24][25][26]. To better understand the role that hormones may play in host defence evolution and variation, however, we need an overarching hypotheses-driven framework that generates testable predictions.…”

Glucocorticoids mediate egg rejection in a brood parasite host

“…So far, the only study that has investigated such links has found a weak 149 positive association between foreign egg acceptance and baseline corticosterone levels [25]. It is therefore 150 unclear if the increased acceptance of model eggs in response to mitotane in this study is mediated by 151 changes in baseline (as in [10]) or parasitism-related stress-induced [9] corticosterone levels. Indeed, our 152 treatment validation design only allowed us to test if mitotane could alleviate a major increase in 153 corticosterone levels in response to captivity stress.…”

“…Host adults show elevated baseline and stress-induced corticosterone levels in response to brood 135 parasitism [9,10]. Until now, the consequences of this endocrine response on host antiparasitic behaviours 136 have been unknown [8].…”

“…Hosts may first evolve endocrine-regulated tolerance or avoidance mechanisms [9,10], either in response 168 to direct or indirect cues and costs of brood parasitism. These mechanisms may then be co-opted to 169 regulate host defences, such as egg rejection.…”

“…For example, host parents caring for a parasitic chick show higher 34 stress-induced corticosterone levels compared to parents caring for only their own young [9]. An increase 35 in the baseline corticosterone levels in hosts can occur directly in response to encountering a foreign egg 36 in the nest [10]. Furthermore, parasitism can alter the endocrine milieu of host offspring, either through an 37 increase in maternally-deposited yolk androgen concentrations [11], or by an increase in the baseline 38 corticosterone levels in host nestlings during competition with parasitic chicks [12].…”