Genetics of affective and anxiety disorders. Annu. Rev. Psychol

Center for Neurobiology and Behavior, Columbia University, New York, New York 10032, USA.
Annual Review of Psychology (Impact Factor: 20.53). 02/2006; 57:117-37. DOI: 10.1146/annurev.psych.57.102904.190118
Source: PubMed

ABSTRACT The study of the genetics of complex behaviors has evolved dramatically from the days of the nature versus nurture debates that dominated much of the past century. Here we discuss advances in our understanding of the genetics of affective and anxiety disorders. In particular, we highlight our growing understanding of specific gene-environment interactions that occur during critical periods in development, setting the stage for later behavioral phenotypes. We review the recent literature in the field, focusing on recent advances in our understanding of the role of the serotonin system in establishing normal anxiety levels during development. We emphasize the importance of understanding the effect of genetic variation at the level of functional circuits and provide examples from the literature of how such an approach has been exploited to study novel genetic endpoints, including genetically based variation in response to medication, a potentially valuable phenotype that has not received much attention to date.

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    • "In this study we also showed that ELF magnetic fi eld exposure at this developmental stage decreases locomotor activity of three-day-old fl ies. Due to the ELF magnetic fi eld exposure at the time of brain development, when the activation of serotonin receptors begins, later reduced locomotor activity may be linked with a possible impact of magnetic fi eld on serotonergic transmission in the brain (Leonardo and Hen 2006). It is well known that serotonin has a role in response to stimuli from environment (Heym et al. 1982, Waterhouse et al. 2004) and that serotonergic neurons are sensitive to changes in behavioral activation (Grahn et al. 1999, Jacobs and Fornal 1999, Portas et al. 2000, Abrams et al. 2004). "
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    International Journal of Radiation Biology 01/2014; 90(5). DOI:10.3109/09553002.2014.888105 · 1.84 Impact Factor
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    • "Regarding the pharmacological knowledge of antidepressants, the choice of KO mice as experimental models of anxiety– depression was remarkably appropriate because it is now well recognized that major depressive disorders result from a combination of genetic and environmental factors. In addition, knowing that anxiety and depression have a high co-morbidity (Gorman and Coplan, 1996; Leonardo and Hen, 2006), it is critical for basic research to develop animal models that present behavioral, neurochemical, and brain morphological phenotypes reminiscent of depression and anxiety. Some " serotonergic " KO mice display important changes in their basal phenotype. "
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    Frontiers in Pharmacology 08/2013; 4:98. DOI:10.3389/fphar.2013.00098 · 3.80 Impact Factor
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    • "Anxiety potentially confounds or contributes to more pronounced cognitive dysfunctions and neuropsychological impairments and/or anatomical changes in depressed individuals (Cameron, Abelson, & Young, 2004; Castaneda, Tuuio- Henriksson, Marttunen, Suvisaari, & Lonnqvist, 2008; Kessler et al., 2003; Leonardo & Hen, 2006). A theoretical review by Eysenck and Calvo (1992) suggests that anxiety hinders memory performance under certain circumstances, as anxious individuals might have less attention capacity for task performance and thus perform worse on working memory tasks demanding effort. "
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