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NeoReviews Vol.7 No.4 2006 e183
© 2006 American Academy of Pediatrics

Stress Hormones and Human Developmental Plasticity

Lessons From Tadpoles

Robert J. Denver, PhD^*
Erica J. Crespi, MS, PhD

^* Department of Molecular, Cellular and Developmental Biology, Department of Ecology and Evolutionary Biology, The University of Michigan, Ann Arbor, Mich
Department of Biology, Vassar College, Poughkeepsie, NY

The first 300 words of the full text of this article appear below.

	Objectives

 
After completing this article, readers should be able to:

1. Define phenotypic plasticity.
   
2. Delineate the roles of stress hormones in controlling the timing of life history transitions and phenotypic outcomes.
   
3. List the long-term phenotypic consequences of exposure to stress early in life.
   

	Introduction

 
Phenotypic expression depends on the interaction between the genotype (nature) and the environment (nurture). This is true for all living organisms, but the physiologic mechanisms that mediate this interaction remain poorly understood. Very early developmental events generally are regarded as being buffered from environmental effects (ie, they are canalized), but it is now clear that the earliest environment experienced by the embryo can shape developmental outcomes, that is, result in developmental plasticity or prenatal programming. For example, the probability of preterm birth is highly correlated with the experience of stress during the periconceptional period. Thus, fetal development tends to be more variable in timing and possibly more susceptible to environmental influences.

	Phenotypic Plasticity

 
The environment influences development by modifying morphology and physiology, thus resulting in specific phenotypic outcomes, and modifying the timing of developmental events. The term "phenotypic plasticity" is used to describe the process by which organisms modify their development, behavior, or physiology in response to changing environments. Phenotypic plasticity has been described in almost every group of plants and animals, and it can have important fitness consequences. For example, it may be adaptive if it leads to increased survival during the embryonic or larval life stage. Yet, there are important tradeoffs associated with phenotypic plasticity. For example, amphibian tadpoles may accelerate metamorphosis in response to a deteriorating larval habitat (eg, a drying pond, high density of predators, low food) and, thus, increase the probability of immediate survival through metamorphosis. However, this accelerated development comes at a cost: decreased growth and smaller body size at transformation that may lead to . . . [Full Text of this Article]