Effects of serotonin precursors on the negative feedback effects of glucocorticoids on hypothalamic-pituitary-adrenal axis function in depression

Maes, Michaël; Meltzer, Herbert Y.; D'Hondt, Peter; Cosyns, Paul; Blockx, P.

doi:10.1016/0306-4530(94)00049-g

Cited by 50 publications

(31 citation statements)

References 69 publications

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“…In the depressed state, elevated cortisol levels may lower l-tryptophan availability, decrease 5-HT turnover, down-regulate presynaptic 5-HT 1A receptors, and upregulate 5-HT 2 receptors. Conversely, serotonin stimulates the secretion of CRH and ACTH and may modulate negative feedback of the HPA axis by glucocorticoids [80]. It has been observed that a lack of CRH-R1 leads to an increase in serotonin levels under basal and stressful conditions [14].…”

Section: Serotonergic Systemmentioning

confidence: 99%

Mechanisms of action of antidepressants: from neurotransmitter systems to signaling pathways

Taylor

Fricker

Devi

et al. 2005

Cellular Signalling

144

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Antidepressants are commonly used in the treatment of anxiety and depression, medical conditions that affect ~17-20% of the population. The clinical effects of antidepressants take several weeks to manifest, suggesting that these drugs induce adaptive changes in brain structures affected by anxiety and depression. In order to develop shorter-acting and more effective drugs for the treatment of anxiety and depression, it is important to understand how antidepressants bring about their beneficial effects. Recent reports suggest that antidepressants can induce neurogenesis in the adult brain, although the mechanisms involved are not clearly understood. In this review, we describe the different neurotransmitter systems that are affected by anxiety and depression and how they are modulated by antidepressant treatment with a focus on signaling molecules and pathways that are activated during neurotransmitter receptor induced neurogenesis.

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Section: Serotonergic Systemmentioning

confidence: 99%

Mechanisms of action of antidepressants: from neurotransmitter systems to signaling pathways

Taylor

Fricker

Devi

et al. 2005

Cellular Signalling

144

View full text Add to dashboard Cite

show abstract

“…There is an extensive literature on cortisol reactivity and the development of mental health disorders [63] and disturbances in HPA regulation have also been associated with affective and anxiety disorders [64][65][66][67]. We suggest that epigenetic differences that perturb the HPA axis could predispose infants to neurobehavioral profiles that interact with postnatal environmental factors leading to later mental health disorders [68].…”

Section: Importance Of This Studymentioning

confidence: 99%

Neurobehavior Related to Epigenetic Differences in Preterm Infants

et al. 2015

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Preterm birth is associated with medical problems affecting the neuroendocrine system, altering cortisol levels resulting in negative effects on newborn neurobehavior. Newborn neurobehavior is regulated by DNA methylation of NR3C1 and HSD11B2. Aim: Determine if methylation of HSD11B2 and NR3C1 is associated with neurobehavioral profiles in preterm infants. Patients & methods: Neurobehavior was measured before discharge from the hospital in 67 preterm infants. Cheek swabs were collected for DNA extraction. Results: Infants with the high-risk neurobehavioral profile showed more methylation than infants with the low-risk neurobehavioral profile at CpG3 for NR3C1 and less methylation of CpG3 for HSD11B2. Infants with these profiles were more likely to have increased methylation of NR3C1 and decreased methylation of HSD11B2 at these CpG sites. Conclusion: Preterm birth is associated with epigenetic differences in genes that regulate cortisol levels related to high-risk neurobehavioral profiles.

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“…Reasons for this gender difference are not clear, but may be related to differences in gonadotropic steroids (Steiner et al 2003). Depression has been correlated with abnormalities in the regulation of neurochemical pathways such as those involving serotonin (Maes et al 1995;Muck-Seler et al 2004;Stockmeier 2003), norepinephrine (Lake et al 1982;Roy et al 1985) and dopamine (Alexopoulos 2001;Pania & Gessab 2002;Ueno 2003). The genetic determination of these pathways may be altered by environmental influences (Grossman et al 2003).…”

mentioning

confidence: 99%

Depressive symptoms in mid‐pregnancy, lifetime stressors and the 5‐HTTLPR genotype

Scheid

Holzman

Jones

et al. 2006

Genes Brain and Behavior

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Few studies of gene-environment interactions for the serotonin transporter promoter polymorphism (5-HTTLPR), life stressors and depression have considered women separately or examined specific types of stressful life events. None have looked at depression during pregnancy. In the Pregnancy Outcomes and Community Health (POUCH) Study, women were queried about history of stressful life events and depressive symptoms at the time of enrollment (15-27 weeks gestation). Stressful life events were grouped a priori into ''subconstructs'' (e.g. economic, legal, abuse, loss) and evaluated by subconstruct, total subconstruct score and total stressful life event score. The effect of genotype on the association between stressful life events and elevated depressive symptoms was assessed in 568 white non-Hispanic participants. The relationship between exposure to abuse and elevated depressive symptoms was more pronounced in the s/s group (OR 5 24.5) than in the s/ l group (OR 5 3.0) and the l/l group (OR 5 7.7), but this significant interaction was detected only after excluding 73 (13%) women with recent use of psychotropic medications. There was no evidence of gene-environment interaction in analytic models with other stressful life events subconstructs, total subconstruct score or total stressful life events score. These data offer modest support to other reports of gene-environment interaction and highlight the importance of considering specific stressful life events.

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Effects of serotonin precursors on the negative feedback effects of glucocorticoids on hypothalamic-pituitary-adrenal axis function in depression

Cited by 50 publications

References 69 publications

Mechanisms of action of antidepressants: from neurotransmitter systems to signaling pathways

Mechanisms of action of antidepressants: from neurotransmitter systems to signaling pathways

Neurobehavior Related to Epigenetic Differences in Preterm Infants

Depressive symptoms in mid‐pregnancy, lifetime stressors and the 5‐HTTLPR genotype

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