Stress, genes and the mechanism of programming the brain for later life

Kloet, E. Ronald de; Sibug, R.M.; Helmerhorst, Frans M.; Schmidt, Mathias V.

doi:10.1016/j.neubiorev.2004.10.008

Cited by 321 publications

(176 citation statements)

References 101 publications

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“…In this way inability to cope with a chronic stressor 153 or exposure to a single acute life event can cause changes in HPA axis activity and corticosteroid action, 154 imposing a risk for depression and other diseases. 131 Prenatal stress.…”

Section: Stressmentioning

confidence: 99%

“…188,189 Human children, as well as rodent pups, are characterized by a stress hypo-responsive period, developing gradually during the first year of life. 154,190 Healthy newborn infants react to stressors with an adrenocortical response, 191 but the HPA axis of a 12-18 months old child does not respond to mild stressors, 192,193 although the child does show a behavioral response to such a stressor. More severe stress, however, will cause an acute rise in corticosterone levels during the stress-hyporesponsive period.…”

Section: Stressmentioning

confidence: 99%

“…198 In rodents, early-life stress induces 5-HTergic dysfunctioning and persistent changes in HPA responsiveness and CRF expression. 131,154,186 Adverse early life experiences appear to interact with chronic stress in adulthood to alter physiology and behavior. 199 The release of corticosterone in response to mild stress is heightened and prolonged in adult male rats that were maternally deprived as pups, indicating impaired glucocorticoid-mediated feedback sensitivity 200 that may results from downregulation of hippocampal GR.…”

Section: Stressmentioning

confidence: 99%

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Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

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In recent years, the term serotonergic vulnerability (SV) has been used in scientific literature, but so far it has not been explicitly defined. This review article attempts to elucidate the SV concept. SV can be defined as increased sensitivity to natural or experimental alterations of the serotonergic (5-HTergic) system. Several factors that may disrupt the 5-HTergic system and hence contribute to SV are discussed, including genetic factors, female gender, personality characteristics, several types of stress and drug use. It is explained that SV can be demonstrated by means of manipulations of the 5-HTergic system, such as 5-HT challenges or acute tryptophan depletion (ATD). Results of 5-HT challenge studies and ATD studies are discussed in terms of their implications for the concept of SV. A model is proposed in which a combination of various factors that may compromise 5-HT functioning in one person can result in depression or other 5-HT-related pathology. By manipulating 5-HT levels, in particular with ATD, vulnerable subjects may be identified before pathology initiates, providing the opportunity to take preventive action. Although it is not likely that this model applies to all cases of depression, or is able to identify all vulnerable subjects, the strength of the model is that it may enable identification of vulnerable subjects before the 5-HT related pathology occurs. Molecular Psychiatry ( Keywords: serotonin; mood disorders; stress; genetics; sex; tryptophan Involvement of serotonin in depressionMood disorders are one of the most prevalent forms of mental illness. 1 According to the DSM-IV, the lifetime risk for major depressive disorder is between 10 and 25% for women and between 5 and 12% for men. 2 Depression has been studied intensively during the last few decades, but the psychological and neurobiological determinants of depression have not yet been precisely defined. Although several factors are known to contribute to the etiology of depression, it is not clear how these factors cause depression, and why some subjects become depressed while others remain unaffected. In terms of biological factors in the etiology of depression, there are several hypotheses. These include neurotransmitter dysfunctions (serotonin, 5-HT; dopamine, DA; norepinephrine, NE); dysregulations in hypothalamic-pituitary-adrenal (HPA) axis activity; and immune system imbalance. The aim of this article is not to discuss all of these hypotheses in detail, but to evaluate the role that serotonin may play within these hypothesized mechanisms.It is widely accepted that diminished serotonergic (5-HTergic) function is involved in the onset and course of depression. 3,4 The 5-HTergic system is a large and complex system. Although nearly all cell bodies of 5-HTergic neurons are located in the raphe nuclei in the brain stem, the axons of these neurons innervate almost the entire brain. The actions of 5-HT are mediated by 16 types and subtypes of receptors. 5 As the 5-HTergic system is assumed to be a modulatory system, the exact func...

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Section: Stressmentioning

confidence: 99%

Section: Stressmentioning

confidence: 99%

Section: Stressmentioning

confidence: 99%

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Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

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“…Cortisol is generally referred to as a classical Bstress hormone^ (Morton et al 1995) and has been implemented as the standard stress indicator in animal welfare research (Mormède et al 2007). Measurably increased cortisol concentrations can be observed from about 3-5 min after the onset of the stressor (Sheriff et al 2011) and peak levels are reached within 15-30 min (De Kloet et al 2005). A cortisol-mediated negative feedback loop causes the system to return to baseline activity again after 60-90 min (Sheriff et al 2011, De Kloet et al 2005.…”

Section: Introductionmentioning

confidence: 99%

“…Measurably increased cortisol concentrations can be observed from about 3-5 min after the onset of the stressor (Sheriff et al 2011) and peak levels are reached within 15-30 min (De Kloet et al 2005). A cortisol-mediated negative feedback loop causes the system to return to baseline activity again after 60-90 min (Sheriff et al 2011, De Kloet et al 2005.…”

Section: Introductionmentioning

confidence: 99%

Cortisol response of wild ungulates to trauma situations: hunting is not necessarily the worst stressor

Gentsch

Kjellander

Röken³

2018

Eur J Wildl Res

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Animal welfare concerns are becoming a central issue in wildlife management and conservation. Thus, we investigated stress response of wild ungulates to potentially traumatic situations (shooting injuries, vehicle collisions, entanglement, injuries or diseases) and hunting methods (stalking, battues and hunts with dogs) by means of serum cortisol concentrations from blood collected from killed animals. Cortisol levels in roe deer ranged below and in wild boar above levels for moose, red deer and fallow deer (hence, pooled as a group Bdeer^). Apart from species, cortisol concentration in trauma situations was mainly explained by trauma type and presence of disturbance after the trauma event. Effect of trauma type differed significantly for Bdeer^, with animals caught in fences and suffering vehicle collisions experiencing higher cortisol levels than animals injured by shooting. Differences between hunting methods were observed in the cervids (Bdeer^and roe deer), with stalking leading to lower cortisol levels than hunts with dogs (both groups) and battues (roe deer). Events both before and after the shot, such as duration of pursuit prior to shooting, location of injury, trauma length and presence of disturbance after the shot were relevant for cortisol levels in hunted cervids. Our results indicate that search teams tracking and euthanising wounded animals should behave in a calm way to minimise disturbance. Still, it is important to acknowledge that many situations described in the literature, i.e. reindeer handling, roe deer captures and red deer yarding, seem even more stressful, beside vehicle collisions, than most hunting methods.

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Cerebral Palsy, Autism Spectrum Disorders, and Developmental Delay in Children Born After Assisted Conception

Hvidtjørn¹,

Schieve²,

Schendel³

et al. 2009

Arch Pediatr Adolesc Med

137

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To assess the existing evidence of associations between assisted conception and cerebral palsy (CP), autism spectrum disorders (ASD), and developmental delay. Data Sources: Forty-one studies identified in a systematical PubMed and Excerpta Medica Database (EMBASE) search for articles published from January 1, 1996, to April 1, 2008. Study Selection: Studies written in English comparing children born after assisted conception with children born after natural conception assessing CP, ASD, and developmental delay, based on original data with a follow-up of 1 year or more. Main Exposures: In vitro fertilization (IVF) with or without intracytoplasmic sperm injection or ovulation induction with or without subsequent intrauterine insemination. Main Outcome Measures: Cerebral palsy, ASD, and developmental delay. Results: Nine CP studies showed that children born after IVF had an increased risk of CP associated with preterm delivery. In our meta-analysis including 19 462 children exposed to IVF, we estimated a crude odds ratio of 2.18 (95% confidence interval, 1.71-2.77). Eight ASD studies and 30 studies on developmental delay showed inconsistent results. No studies assessed the risk of CP, ASD, or developmental delay in children born after ovulation induction exclusively.

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Stress, genes and the mechanism of programming the brain for later life

Cited by 321 publications

References 101 publications

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

Cortisol response of wild ungulates to trauma situations: hunting is not necessarily the worst stressor

Cerebral Palsy, Autism Spectrum Disorders, and Developmental Delay in Children Born After Assisted Conception

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