Early Fasting Is Long Lasting: Differences in Early Nutritional Conditions Reappear under Stressful Conditions in Adult Female Zebra Finches

Conditions experienced during early life can have profound effects on individual development and condition in adulthood. Differences in nutritional provisioning in birds during the first month of life can lead to differences in growth, reproductive success and survival. Yet, under natural conditions shorter periods of nutritional stress will be more prevalent. Individuals may respond differently, depending on the period of development during which nutritional stress was experienced. Such differences may surface specifically when poor environmental conditions challenge individuals again as adults. Here, we investigated long term consequences of differences in nutritional conditions experienced during different periods of early development by female zebra finches (Taeniopygia guttata) on measures of management and acquisition of body reserves. As nestlings or fledglings, subjects were raised under different nutritional conditions, a low or high quality diet. After subjects reached sexual maturity, we measured their sensitivity to periods of food restriction, their exploration and foraging behaviour as well as adult resting metabolic rate (RMR). During a short period of food restriction, subjects from the poor nutritional conditions had a higher body mass loss than those raised under qualitatively superior nutritional conditions. Moreover, subjects that were raised under poor nutritional conditions were faster to engage in exploratory and foraging behaviour. But RMR did not differ among treatments. These results reveal that early nutritional conditions affect adult exploratory behaviour, a representative personality trait, foraging and adult's physiological condition. As early nutritional conditions are reflected in adult phenotypic plasticity specifically when stressful situations reappear, the results suggest that costs for poor developmental conditions are paid when environmental conditions deteriorate

Compensatory Development and Costs of Plasticity: Larval Responses to Desiccated Conspecifics

Understanding constraints on phenotypic plasticity is central to explaining its evolution and the evolution of phenotypes in general, yet there is an ongoing debate on the classification and relationships among types of constraints. Since plasticity is often a developmental process, studies that consider the ontogeny of traits and their developmental mechanisms are beneficial. We manipulated the timing and reliability of cues perceived by fire salamander larvae for the future desiccation of their ephemeral pools to determine whether flexibility in developmental rates is constrained to early ontogeny. We hypothesized that higher rates of development, and particularly compensation for contradictory cues, would incur greater endogenous costs. We found that larvae respond early in ontogeny to dried conspecifics as a cue for future desiccation, but can fully compensate for this response in case more reliable but contradictory cues are later perceived. Patterns of mortality suggested that endogenous costs may depend on instantaneous rates of development, and revealed asymmetrical costs of compensatory development between false positive and false negative early information. Based on the results, we suggest a simple model of costs of development that implies a tradeoff between production costs of plasticity and phenotype-environment mismatch costs, which may potentially underlie the phenomenon of ontogenetic windows constraining plasticity

Heat Shock Proteins and Amateur Chaperones in Amyloid-Beta Accumulation and Clearance in Alzheimer’s Disease

The pathologic lesions of Alzheimer’s disease (AD) are characterized by accumulation of protein aggregates consisting of intracellular or extracellular misfolded proteins. The amyloid-β (Aβ) protein accumulates extracellularly in senile plaques and cerebral amyloid angiopathy, whereas the hyperphosphorylated tau protein accumulates intracellularly as neurofibrillary tangles. “Professional chaperones”, such as the heat shock protein family, have a function in the prevention of protein misfolding and subsequent aggregation. “Amateur” chaperones, such as apolipoproteins and heparan sulfate proteoglycans, bind amyloidogenic proteins and may affect their aggregation process. Professional and amateur chaperones not only colocalize with the pathological lesions of AD, but may also be involved in conformational changes of Aβ, and in the clearance of Aβ from the brain via phagocytosis or active transport across the blood–brain barrier. Thus, both professional and amateur chaperones may be involved in the aggregation, accumulation, persistence, and clearance of Aβ and tau and in other Aβ-associated reactions such as inflammation associated with AD lesions, and may, therefore, serve as potential targets for therapeutic intervention

Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection

The potential for ischemic preconditioning to reduce infarct size was first recognized more than 30 years ago. Despite extension of the concept to ischemic postconditioning and remote ischemic conditioning and literally thousands of experimental studies in various species and models which identified a multitude of signaling steps, so far there is only a single and very recent study, which has unequivocally translated cardioprotection to improved clinical outcome as the primary endpoint in patients. Many potential reasons for this disappointing lack of clinical translation of cardioprotection have been proposed, including lack of rigor and reproducibility in preclinical studies, and poor design and conduct of clinical trials. There is, however, universal agreement that robust preclinical data are a mandatory prerequisite to initiate a meaningful clinical trial. In this context, it is disconcerting that the CAESAR consortium (Consortium for preclinicAl assESsment of cARdioprotective therapies) in a highly standardized multi-center approach of preclinical studies identified only ischemic preconditioning, but not nitrite or sildenafil, when given as adjunct to reperfusion, to reduce infarct size. However, ischemic preconditioning—due to its very nature—can only be used in elective interventions, and not in acute myocardial infarction. Therefore, better strategies to identify robust and reproducible strategies of cardioprotection, which can subsequently be tested in clinical trials must be developed. We refer to the recent guidelines for experimental models of myocardial ischemia and infarction, and aim to provide now practical guidelines to ensure rigor and reproducibility in preclinical and clinical studies on cardioprotection. In line with the above guideline, we define rigor as standardized state-of-the-art design, conduct and reporting of a study, which is then a prerequisite for reproducibility, i.e. replication of results by another laboratory when performing exactly the same experiment

Anti-brood parasite defences : the role of individual and social learning

In this chapter, we consider the ways in which learning is involved in the antibrood parasitism defences that hosts deploy across the nesting cycle. Brood parasitism varies in space and through time, and hosts have accordingly evolved plastic defences that can be tuned to local conditions. Hosts can achieve their defence plasticity by individual and social learning, as well as by experienceindependent mechanisms. While these mechanisms can profoundly affect the coevolutionary dynamics between hosts and their brood parasites, our understanding of how they feature across the host nesting cycle is far from complete. Hosts can actively defend themselves against brood parasitism via a variety of behaviours, including nest defence, egg discrimination and chick discrimination. Such anti-brood parasite defences rely on the host ’ s ability to recognise and then defend against the parasitic threat, and there is good evidence that both these components of discrimination can be in fl uenced by learning. To date, most research has focused on the function of learning in nest defence, but the learning mechanisms underlying egg discrimination are much better understood; and despite some notable exceptions, the role of learning in chick discrimination remains largely unexplored. An important challenge now is to understand the observed plasticity of anti-brood parasite defences in the context of environmental heterogeneity and speci fi cally in terms of variation in the presence, detection and reliability of parasitism cues

Anti-brood Parasite Defences: The Role of Individual and Social Learning

In this chapter, we consider the ways in which learning is involved in the antibrood parasitism defences that hosts deploy across the nesting cycle. Brood parasitism varies in space and through time, and hosts have accordingly evolved plastic defences that can be tuned to local conditions. Hosts can achieve their defence plasticity by individual and social learning, as well as by experienceindependent mechanisms. While these mechanisms can profoundly affect the coevolutionary dynamics between hosts and their brood parasites, our understanding of how they feature across the host nesting cycle is far from complete. Hosts can actively defend themselves against brood parasitism via a variety of behaviours, including nest defence, egg discrimination and chick discrimination. Such anti-brood parasite defences rely on the host’s ability to recognise and then defend against the parasitic threat, and there is good evidence that both these components of discrimination can be influenced by learning. To date, most research has focused on the function of learning in nest defence, but the learning mechanisms underlying egg discrimination are much better understood; and despite some notable exceptions, the role of learning in chick discrimination remains largely unexplored. An important challenge now is to understand the observed plasticity of anti-brood parasite defences in the context of environmental heterogeneity and specifically in terms of variation in the presence, detection and reliability of parasitism cues