Vergne DE, Nemeroff CB. The interaction of serotonin transporter gene polymorphisms and early adverse life events on vulnerability for major depression. Curr Psychiatry Rep 8: 447-452

Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Suite 4000 WMRB, 101 Woodruff Circle, Atlanta, GA 30322, USA.
Current Psychiatry Reports (Impact Factor: 3.24). 01/2007; 8(6):452-7. DOI: 10.1007/s11920-006-0050-y
Source: PubMed


Considerable literature supports the hypothesis of dysfunction in central nervous system serotonergic circuits in the pathophysiology of mood disorders, specifically major depression. Since the development of the selective serotonin (5-HT) reuptake inhibitors, a putative role for the 5-HT transporter (SERT) in the etiology of depression has been explored. The discovery of a functional SERT polymorphism has provided a novel tool to further scrutinize the role of serotonergic neurons in depression. This article reviews the burgeoning evidence of an interaction between early life stress and an SERT polymorphism on vulnerability to depression.

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Available from: Charles B Nemeroff
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    • "Whereas glutamatergic and GABAergic systems are implicated in anxiety, learning and memory processes (Roozendaal et al., 2009), serotonin (5-HT), due to the important functions it play mainly -but not only-within the amygdala , 5-HT has a regulatory role in the anxiety behaviors and among the fifteen serotonin receptors, 5-HT1A and 5-HT2C receptors are relatively abundant in the amygdala (Li et al., 2012). Moreover, polymorphisms of the gene coding for the serotonin transporter have been linked to stress induced depression (Caspi et al., 2003; Vergne and Nemeroff, 2006). In pharmacology, 5-HT1A receptor agonists, such as buspirone due to its anxiolytic effects, have constituted an anxiolytic drug (De Vry, 1995; Li et al., 2012). "
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    • "While the annual prevalence of depression as defined by the Diagnostic and Statistical Manual IV-TR (DSM-IV-TR)22 criteria is estimated to be 3.2%, the heritability of depression is thought to be 31%–42%.23 In 2003, a gene × environment (G × E) hypothesis was proposed, suggesting that because an association between 5-HTT genotype and response to stress in animals and humans had been demonstrated, and that stressful life events are known to affect the onset and course of depression,24 it was therefore logical to conclude that the 5-HTT genotype could contribute to the development of depression.7 These researchers sought to determine if 5-HTT genotype altered the serotonergic response to stress, thereby predisposing participants to a greater influence of stressful life events on depression.7 Caspi et al demonstrated a positive association between the number of stressful life events and the probability of depression that was statistically stronger in S carriers than L homozygotes.7 "
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