Genetics of affective and anxiety disorders. Annu. Rev. Psychol
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.
- SourceAvailable from: Danica Zmejkoski (former Dimitrijevic)
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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). "
ABSTRACT: Abstract Purpose: Extremely low frequency (ELF) magnetic fields are essential ecological factor which may induce changes in many organisms. The aim of this study was to examine the effects in Drosophila subobscura exposed for 48 h to ELF magnetic field (50 Hz, 0.5 mT) at different developmental stages. Materials and methods: Egg-first instar larvae developmental stage of D. subobscura isofemale lines was exposed to ELF magnetic field, and fitness components (developmental time, developmental dynamics, viability and sex ratio) and locomotor activity of 3-days old males and females were monitored. Also, just eclosed D. subobscura isofemale adults were exposed to ELF magnetic field and their locomotor activity was monitored just after. Results: ELF magnetic field shortens developmental time, increases viability and does not affect sex ratio of D. subobscura. No matter which developmental stage is exposed, ELF magnetic field significantly decreases locomotor activity of adult flies, but after exposure of just eclosed adults observed change lasts longer. Conclusions: Applied ELF magnetic field modifies fitness components and locomotor activity of D. subobscura. Observed effects can be attributed to the influence of magnetic field on different stages of development where the hormonal and nervous systems play important role in the control of examined parameters.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. "
ABSTRACT: Why antidepressants vary in terms of efficacy is currently unclear. Despite the leadership of Selective serotonin reuptake inhibitors (SSRIs) in the treatment of depression, the precise neurobiological mechanisms involved in their therapeutic action are poorly understood. A better knowledge of molecular interactions between monoaminergic system, pre- and post-synaptic partners, brain neuronal circuits and regions involved may help to overcome limitations of current treatments and to identify new therapeutic targets. Intracerebral in vivo microdialysis (ICM) already provided important information about the brain mechanism of action of antidepressants first in anesthetized rats in the early 90s, and since then in conscious wild-type or knockout mice. The principle of ICM is based on the balance between release of neurotransmitters (e.g., monoamines,) and re-uptake by selective transporters (e.g., SERT for serotonin 5-HT). Complementary to electrophysiology, this technique reflects presynaptic monoamines release and intrasynaptic events corresponding to ≈ 80% of whole brain tissue content. The inhibitory role of serotonergic autoreceptors infers that they limit somatodendritic and nerve terminal 5-HT release. It has been proposed that activation of 5-HT1A and 5-HT1B receptor sub-types limit the antidepressant-like activity of Selective Serotonin Reuptake Inhibitors (SSRI). This hypothesis is based partially on results obtained in ICM experiments performed in naïve, non-stressed Rodents. The present review will first remind the principle and methodology of ICM performed in mice. The crucial need of developing animal models that display anxiety and depression-like behaviors, neurochemical and brain morphological phenotypes reminiscent of these mood disorders in Human, will be underlined. Recently developed genetic mouse models have been generated to independently manipulate 5-HT1A auto and hetero-receptors and ICM helped to clarify the role of the presynaptic componentFrontiers 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. "
ABSTRACT: The aim of this study was to examine both executive control of verbal working memory and verbal learning as well as long-term storage function in outpatients with major depressive disorder (n = 61) compared to healthy controls (n = 92). A total of 37 patients had no co-morbid anxiety disorder, whereas 24 had a co-morbid anxiety disorder. Both patient groups showed impaired working memory test performance compared to healthy controls. Patients with co-morbid depression and anxiety disorder performed significantly below the depression group. Only patients with depression and co-morbid anxiety displayed deficient long-term memory function compared to healthy controls. The present results show impairments in various memory functions in patients presenting depression and depression with co-morbid anxiety disorder.The Clinical Neuropsychologist 03/2011; 25(3):359-75. DOI:10.1080/13854046.2010.547518 · 1.58 Impact Factor