COBRE: UID: PILOT: SELENIUM HOMEOSTASIS AND ANXIETY: THE ROLE OF THE GENOTYPE

点击翻译按钮获取中文摘要

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Selenium (Se) is an essential trace element that is critical for maintaining normal brain function in humans and other vertebrates. Se deficiency causes numerous neurological and physiological deficits, eliciting considerable interest regarding the potential benefits of Se supplementation. In particular, there is some evidence that Se supplementation has beneficial mental health effects in humans, including decreased anxiety. However, the effects of Se supplementation on human behavior and mood are controversial; while several studies have linked Se status to anxiety, others have found no such effect. We hypothesize that a genotype by environment interaction may explain the conflicting results regarding the efficacy of Se supplementation in humans. While the concept of a genotype by environment interaction is not new to evolutionary biologists, genetic variation among individuals and populations is only now becoming a key factor in effective medical treatment (i.e. "personalized medicine"). Studying the genetic basis and evolutionary relevance of genetic variation in the response to Se supplementation is difficult in humans, necessitating an approach using model organisms. Here we argue that our behaviorally distinct strains of zebrafish are the ideal model system in which the genetic basis of a population specific response to Se supplementation can be studied.