A growing body of evidence from across taxa suggests that exposure to elevated levels of glucocorticoids during early development can have long-term effects upon physiological and behavioral phenotypes. Additionally, there is some, though limited, evidence that similar early exposure can also negatively impact cognitive ability. Following pioneering mammalian studies, several avian studies have revealed that the responsiveness of the hypothalamo-pituitary-adrenal (HPA) axis as an adult can be explained by levels of corticosterone, the avian glucocorticoid, the individual experienced as a nestling or even as an embryo via yolk exposure. Studies also suggest that perinatal exposure to corticosterone can have effects upon avian ‘personalities’ or coping styles, and findings from mammalian studies suggest that these long-term effects are mediated epigenetically via altered expression of relevant DNA sequences. Although a consistent pattern across-species has yet to emerge, recent work in Florida scrub-jays Aphelocoma coerulescens found that baseline corticosterone levels in 11-day-old nestlings explained 84% of the variation in ‘personality’ (bold vs. timid) when those individuals were tested approximately seven months later. Nestlings with elevated corticosterone levels were more timid than those individuals that as nestlings experienced relatively low corticosterone levels. Some researchers have suggested that parents might use such mechanisms to ‘program’ their offsprings’ phenotype to best fit prevailing environmental conditions. This review will visit what is known about the links between stressful developmental conditions that result in exposure to elevated corticosterone and the short- and long-term effects of this steroid hormone upon central nervous system function and whether alterations thereof are beneficial, deleterious, or neutral. It will concentrate on examples from birds, although critical supporting studies from the mammalian literature will be included as appropriate.
The immune system is a necessary, but potentially costly, defense against infectious diseases. When nutrition is limited, immune activity may consume a significant amount of an organism's energy budget. Levels of dietary protein affect immune system function; high levels can enhance disease resistance. We exposed southern leopard frog [Lithobates sphenocephalus (=Rana sphenocephala)] tadpoles to high and low protein diets crossed with the presence or absence of the pathogenic amphibian chytrid fungus (Batrachochytrium dendrobatidis; Bd) and quantified: (1) tadpole resistance to Bd; (2) tadpole skin-swelling in response to phytohaemagglutinin (PHA) injection (a measure of the T cell-mediated response of the immune system); (3) bacterial killing ability (BKA) of tadpole blood (a measure of the complement-mediated cytotoxicity of the innate immune system); and (4) tadpole growth and development. Tadpoles raised on a low-protein diet were smaller and less developed than tadpoles on a high-protein diet. When controlled for developmental stage, tadpoles raised on a low-protein diet had reduced PHA and BKA responses relative to tadpoles on a high-protein diet, but these immune responses were independent of Bd exposure. High dietary protein significantly increased resistance to Bd. Our results support the general hypothesis that host condition can strongly affect disease resistance; in particular, fluctuations in dietary protein availability may change how diseases affect populations in the field.
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