Corticosterone and foraging behaviour in a pelagic seabird

Because endocrine mechanisms are thought to mediate behavioral responses to changes in the environment, examining these mechanisms is essential for understanding how long-lived seabirds adjust their foraging decisions to contrasting environmental conditions in order to maximize their fitness. In this context, the hormone corticosterone (CORT) deserves specific attention because of its major connections with locomotor activities. We examined for the first time the relationships between individual CORT levels and measurements of foraging success and behavior using satellite tracking and blood sampling from wandering albatrosses (Diomedea exulans) before (pretrip CORT levels) and after (posttrip CORT levels) foraging trips during the incubation period. Plasma CORT levels decreased after a foraging trip, and the level of posttrip CORT was negatively correlated with individual foraging success, calculated as total mass gain over a foraging trip. Pretrip CORT levels were not linked to time spent at sea but were positively correlated with daily distance traveled and maximum range at sea. In this study, we were able to highlight the sensitivity of CORT levels to variation in energy intake, and we showed for the first time that individual CORT levels can be explained by variation in foraging success. Relationships between pretrip CORT levels and daily distance traveled and maximum range were independent of pretrip body mass, suggesting that slight elevations in pretrip CORT levels might facilitate locomotor activity. However, because both foraging behavior and pretrip CORT levels could be affected by individual quality, future experimental studies including manipulation of CORT levels are needed to test whether CORT can mediate foraging decisions according to foraging conditions

An experimental manipulation of life-history trajectories and resistance to oxidative stress.

Optimal investment into life-history traits depends on the environmental conditions that organisms are likely to experience during their life. Evolutionary theory tells us that optimal investment in reproduction versus maintenance is likely to shape the pattern of age-associated decline in performance, also known as aging. The currency that is traded against different vital functions is, however, still debated. Here, we took advantage of a phenotypic manipulation of individual quality in early life to explore (1) long-term consequences on life-history trajectories, and (2) the possible physiological mechanism underlying the life-history adjustments. We manipulated phenotypic quality of a cohort of captive zebra finches (Taeniopygia guttata) by assigning breeding pairs to either an enlarged or a reduced brood. Nestlings raised in enlarged broods were in poorer condition than nestlings raised in reduced broods. Interestingly, the effect of environmental conditions experienced during early life extended to the age at first reproduction. Birds from enlarged broods delayed reproduction. Birds that delayed reproduction produced less offspring but lived longer, although neither fecundity nor longevity were directly affected by the experimental brood size. Using the framework of the life-table response experiment modeling, we also explored the effect of early environmental condition on population growth rate and aging. Birds raised in reduced broods tended to have a higher population growth rate, and a steeper decrease of reproductive value with age than birds reared in enlarged broods. Metabolic resources necessary to fight off the damaging effect of reactive oxygen species (ROS) could be the mechanism underlying the observed results, as (1) birds that engaged in a higher number of breeding events had a weaker red blood cell resistance to oxidative stress, (2) red blood cell resistance to oxidative stress predicted short-term mortality (but not longevity), and (3) was related with a parabolic function to age. Overall, these results highlight that early condition can have long-term effects on life-history trajectories by affecting key life-history traits such as age at first reproduction, and suggest that the trade-off between reproduction and self-maintenance might be mediated by the cumulative deleterious effect of ROS

Ambient temperature and pregnancy influence cortisol levels in female guinea pigs and entail long-term effects on the stress response of their offspring

a b s t r a c t Mammals generally respond to the important metabolic requirements imposed by thermoregulation and pregnancy by increasing plasma concentrations of glucocorticoid that promote the mobilization of body reserves and enhance energy use by tissues. This study examined the impact of distinct ambient temperatures and reproductive status on cortisol plasma levels in female guinea pigs (Cavia aperea f. porcellus). We also examined cortisol profiles of their offspring. Forty adult females were placed in individual boxes, 20 were exposed to a neutral thermal regime (mean ambient temperature 22.1 ± 1.5°C) and 20 were maintained under a cool thermal regime (15.1 ± 1.5°C). Within each treatment, 12 females were pregnant and 8 were non-pregnant. Pregnancy generated a marked elevation of baseline cortisol. Ambient temperature also affected cortisol concentrations. Compared to the pregnant females from the neutral thermal regime, pregnant females maintained under cool conditions exhibited lower baseline levels of cortisol, were less active, but they displayed a greater stress response (i.e. rapid increase of plasma cortisol) following handling. Thermal treatment did not influence reproductive output, reproductive effort, or offspring characteristics. This suggests that pregnant female guinea pigs cope with cool (but not extreme) thermal conditions by reducing activity and baseline cortisol levels, possibly to save energy via an adaptive response. Interestingly, the greater amplitude of the stress response of the cool regime females was also observed in their offspring 2 months after parturition, suggesting that hormonal ambience experienced by the individuals in utero shaped their stress response long after birth

Prolactin stress response does not predict brood desertion in a polyandrous shorebird

One of the fundamental principles of the life-history theory is that parents need to balance their resources between current and future offspring. Deserting the dependent young is a radical life-history decision that saves resources for future reproduction but that may cause the current brood to fail. Despite the importance of desertion for reproductive success, and thus fitness, the neuroendocrine mechanisms of brood desertion are largely unknown. We investigated two candidate hormones that may influence brood desertion in the Kentish plover Charadrius alexandrinus: prolactin ('parental hormone') and corticosterone ('stress hormone'). Kentish plovers exhibit an unusually diverse mating and parental care system: brood desertion occurs naturally since either parent (the male or the female) may desert the brood after the chicks hatch and mate with a new partner shortly after. We measured the hormone levels of parents at hatching using the standard capture and restraint protocol. We subsequently followed the broods to determine whether a parent deserted the chicks. We found no evidence that either baseline or stress-induced prolactin levels of male or female parents predicted brood desertion. Although stress-induced corticosterone levels were generally higher in females compared with males, individual corticosterone levels did not explain the probability of brood desertion. We suggest that, in this species, low prolactin levels do not trigger brood desertion. In general, we propose that the prolactin stress response does not reflect overall parental investment in a species where different parts of the breeding cycle are characterized by contrasting individual investment strategies. (C) 2012 Elsevier Inc. All rights reserved

Genetic characterization of Erve virus, a European Nairovirus distantly related to Crimean-Congo hemorrhagic fever virus

Erve virus (ERVEV) is a European Nairovirus that is suspected to cause severe headache (thunderclap headache) and intracerebral hemorrhage. The mode of transmission to humans (ticks or mosquitoes) is still unknown. Currently, no standardized testing method for ERVEV exists and only a small partial sequence of the polymerase gene is available. Here, we present the first complete genome sequence of ERVEV S, M, and L segments. Phylogenetic comparison of the amino acid sequence of the L-protein (RNA-dependent RNA polymerase) revealed only 48 % homology to available L-protein sequences of other Nairoviruses like Crimean-Congo hemorrhagic fever virus, Nairobi sheep disease virus, Hazara virus, Kupe virus, and Dugbe virus. Among themselves, these Nairoviruses show 62-89 % homology in the L-protein sequences. Therefore, ERVEV seems to be only distantly related to other Nairoviruses. The new sequence data can be used for the development of diagnostic methods and the identification of the natural vector

Natural history of murine gamma-herpesvirus infection

Murine gamma-herpesvirus 68 (MHV-68) is a natural pathogen of small rodents and insectivores (mice, voles and shrews). The primary infection is characterized by virus replication in lung epithelial cells and the establishment of a latent infection in B lymphocytes. The virus is also observed to persist in lung epithelial cells, dendritic cells and macrophages. Splenomegaly is observed two weeks after infection, in which there is a CD4+ T-cell-mediated expansion of B and T cells in the spleen. At three weeks post-infection an infectious mononucleosis-like syndrome is observed involving a major expansion of Vbeta4+CD8+ T cells. Later in the course of persistent infection, ca. 10% of mice develop lymphoproliferative disease characterized as lymphomas of B-cell origin. The genome from MHV-68 strain g2.4 has been sequenced and contains ca. 73 genes, the majority of which are collinear and homologous to other gamma-herpesviruses. The genome includes cellular homologues for a complement-regulatory protein, Bcl-2, cyclin D and interleukin-8 receptor and a set of novel genes M1 to M4. The function of these genes in the context of latent infections, evasion of immune responses and virus-mediated pathologies is discussed. Both innate and adaptive immune responses play an active role in limiting virus infection. The absence of type I interferon (IFN) results in a lethal MHV-68 infection, emphasizing the central role of these cytokines at the initial stages of infection. In contrast, type II IFN is not essential for the recovery from infection in the lung, but a failure of type II IFN receptor signalling results in the atrophy of lymphoid tissue associated with virus persistence. Splenic atrophy appears to be the result of immunopathology, since in the absence of CD8+ T cells no pathology occurs. CD8+ T cells play a major role in recovery from the primary infection, and also in regulating latently infected cells expressing the M2 gene product. CD4+ T cells have a key role in surveillance against virus recurrences in the lung, in part mediated through 'help' in the genesis of neutralizing antibodies. In the absence of CD4+ T cells, virus-specific CD8+ T cells are able to control the primary infection in the respiratory tract, yet surprisingly the memory CD8+ T cells generated are unable to inhibit virus recurrences in the lung. This could be explained in part by the observations that this virus can downregulate major histocompatibility complex class I expression and also restrict inflammatory cell responses by producing a chemokine-binding protein (M3 gene product). MHV-68 provides an excellent model to explore methods for controlling gamma-herpesvirus infection through vaccination and chemotherapy. Vaccination with gp150 (a homologue of gp350 of Epstein-Barr virus) results in a reduction in splenomegaly and virus latency but does not block replication in the lung, nor the establishment of a latent infection. Even when lung virus infection is greatly reduced following the action of CD8+ T cells, induced via a prime-boost vaccination strategy, a latent infection is established. Potent antiviral compounds such as the nucleoside analogue 2'deoxy-5-ethyl-beta-4'-thiouridine, which disrupts virus replication in vivo, cannot inhibit the establishment of a latent infection. Clearly, devising strategies to interrupt the establishment of latent virus infections may well prove impossible with existing methods