Prenatal stress diminishes neurogenesis in the dentate gyrus of juvenile Rhesus monkeys

Coe, Christopher L.; Kramer, Marian; Czéh, Boldizsár; Gould, Elizabeth; Reeves, Alison J.; Kirschbaum, Clemens; Fuchs, Eberhard

doi:10.1016/s0006-3223(03)00698-x

Cited by 410 publications

(320 citation statements)

References 72 publications

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“…A recent study in monkeys suggested that this relationship is mediated through dopamine and dopamine receptors (Schneider et al, 2008). As such antenatal maternal anxiety may influence early neuronal developmental patterns leading to alterations in brain circuitry or synaptic functioning (Coe et al, 2003). This may happen through hormones released by the mother during anxious periods that enter the fetus through the placenta and umbilical cord (Nathanielsz, 1999;Gitau et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Developmental brain alterations in 17 year old boys are related to antenatal maternal anxiety

Mennes

Bergh

Lagae

et al. 2009

Clinical Neurophysiology

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General rightsCopyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.-Users may download and print one copy of any publication from the public portal for the purpose of private study or research -You may not further distribute the material or use it for any profit-making activity or commercial gain -You may freely distribute the URL identifying the publication in the public portal Take down policy If you believe that this document breaches copyright, please contact us providing details, and we will remove access to the work immediately and investigate your claim. a b s t r a c tObjective: To assess the association between maternal anxiety during pregnancy and the brain activity of 17 year old adolescents performing two cognitive control tasks. Methods: Twenty-three 17 year old boys of mothers whose level of anxiety was measured during pregnancy were investigated using ERP while performing a Go/Nogo paradigm assessing exogenous cognitive control and a Gambling paradigm requiring endogenous cognitive control. Results: No effects of antenatal maternal anxiety were observed in the Go/Nogo paradigm. However, in the Gambling paradigm adolescents of the high anxiety group (n = 8) showed a less efficient pattern of decision making compared to the adolescents in the low-average anxiety group (n = 15). Moreover, only for this task the ERP data showed an enlarged early frontal P2a component in the high anxiety group. Conclusions: The brain activity of adolescents during an endogenous cognitive control task is associated to the level of anxiety experienced by their mother during pregnancy. This association was not observed during an exogenous cognitive control task. Significance: This study indicates that a child's brain functionality is related to its mother's anxiety during pregnancy. Endogenous cognitive control is regarded the cognitive function most affected by the level of antenatal maternal anxiety.

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Section: Discussionmentioning

confidence: 99%

Developmental brain alterations in 17 year old boys are related to antenatal maternal anxiety

Mennes

Bergh

Lagae

et al. 2009

Clinical Neurophysiology

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“…Moreover, in humans there is a positive linear relationship between maternal and prenatal concentrations of cortisol (Gitau, Cameron, Fisk, & Glover, 1998). Rodent studies suggest that prenatal stress affects several areas of the developing brain, including the hippocampus, septum, amygdala, and frontal cortex (Coe et al, 2003;McCormick, Smythe, Sharma, & Meaney, 1995;Uno et al, 1990;Weinstock, 2001). Prenatal stress is also known to affect concentrations of DA, norepinephrine (NE), and serotonin (5-HT) in brain areas of adult rats either chronically stressed or under stress challenge (Fride & Weinstock, 1988;Peters, 1982Peters, , 1990Takahashi, Turner, & Kalin, 1992;Weinstock, 2001).…”

Section: Discussionmentioning

confidence: 99%

Sensory Processing Disorder in a Primate Model: Evidence From a Longitudinal Study of Prenatal Alcohol and Prenatal Stress Effects

et al. 2008

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Disrupted sensory processing, characterized by over-or underresponsiveness to environmental stimuli, has been reported in children with a variety of developmental disabilities. This study examined the effects of prenatal stress and moderate-level prenatal alcohol exposure on tactile sensitivity and its relationship to striatal dopamine system function in thirty-eight 5-to 7-year-old rhesus monkeys. The monkeys were from four experimental conditions: (a) prenatal alcohol exposed, (b) prenatal stress, (c) prenatal alcohol exposed + prenatal stress, and (d) sucrose controls. Increased D 2 receptor binding in the striatum, evaluated using positron emission tomography neuroimaging, was related to increased withdrawal (aversion) responses to repetitive tactile stimuli and reduced habituation across trials. Moreover, prenatal stress significantly increased overall withdrawal responses to repetitive tactile stimulation compared to no prenatal stress.Sensory processing disorders, characterized by under-or overresponsiveness to sensory stimulation that most individuals perceive as harmless (Ayres & Robbins, 1979) NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript estimated to occur in 5% of the general population (Ahn, Miller, Milberger, & McIntosh, 2004) and seem to pose a unique challenge for people with developmental disabilities (Baranek, 2002), including autism, attention deficit hyperactivity disorder (ADHD), fragile X syndrome, and other developmental disabilities (Ayres & Tickle, 1980;Baranek, 1999;Baranek & Berkson, 1994;Baranek, Foster, & Berkson, 1997;Cermak & Daunhauer, 1997;Grandin, 1992;Kinnealey, 1973;Larson, 1982;Mangeot et al., 2001;Miller et al., 1999). Understanding the neurobiological processes associated with sensory processing disruptions is important to developing appropriate preventative and intervention approaches.This study examined whether disrupted sensory processing occurs in monkeys as a result of prenatal exposure to alcohol and/or stress, and if so, whether it would be associated with dopamine functioning in the striatum assessed with positron emission tomography (PET) neuroimaging. We employed a primate model for these studies because in human studies causal conclusions are difficult to reach due to confounding variables. Even with the best statistical analyses it is difficult, if not impossible, to separate completely the effects of variables associated with alcohol use, such as psychological stress, tobacco use, or chaotic home life, from the effects of fetal alcohol exposure per se. Nonhuman primates also have the advantage of gestation characteristics and early development similar to the human, and their shorter life span makes longitudinal studies somewhat easier to conduct. Rhesus monkeys were used because of the large amount of available data on their behavior and development in laboratory settings (Harlow & Harlow, 1969;Suomi, 1997) A. Jean Ayres (1964), an occupational therapist and educational psychologist, coined the term "tactile defensiveness" t...

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“…Elevated glucocorticoid levels also endanger cells in the neonatal brain as evidenced by decreased hippocampal volume (Coe et al, 2003) and retarded overall brain growth and neurological development (Flagel et al, 2002). Postnatal DEX treatment decreases both the number and size of cortical neurons (Kreider et al, 2006), which persists into adulthood as these rats show altered social behavior and learning and memory deficits (Kamphuis et al, 2004, Neal et al, 2004.…”

Section: Nih Public Accessmentioning

confidence: 99%

Glucocorticoids exacerbate hypoxia-induced expression of the pro-apoptotic gene Bnip3 in the developing cortex

Sandau

Handa

2007

Neuroscience

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Neonatal administration of the synthetic glucocorticoid, dexamethasone (DEX) retards brain growth, alters adult behaviors and induces cell death in the rat brain, thereby implicating glucocorticoids as developmentally neuroendangering compounds. Glucocorticoids also increase expression of proapoptotic Bcl-2 family members and exacerbate expression of hypoxic responsive genes. Bnip3 is a pro-apoptotic Bcl-2 family member that is upregulated in response to hypoxia. In these studies, we investigated the interactions of glucocorticoid receptor and hypoxia in the regulation of Bnip3 mRNA in cortical neurons. Using quantitative real time RT-PCR, we found that DEX treatment of postnatal day 4-6 rat pups caused a significant increase in Bnip3 mRNA expression compared to vehicle controls. A significant increase in Bnip3 mRNA was also measured in primary cortical neurons 72 hours after treatment with RU28362, a glucocorticoid receptor selective agonist. In primary cortical neurons, hypoxia increased Bnip3 mRNA expression and this was exacerbated with RU28362 treatment. To elucidate the mechanism of glucocorticoid and hypoxia mediated regulation of Bnip3 transcription, a Bnip3 promoter -luciferase reporter construct was utilized in primary cortical neurons. Upregulation of the Bnip3 promoter was mediated by a single glucocorticoid response element and a hypoxic response element. Bnip3 overexpression in primary cortical neurons significantly increased cell death, which is dependent on the Bnip3 transmembrane domain. However, despite the increased expression of Bnip3 following glucocorticoid and hypoxia treatment, corresponding decreases in cell survival were minimal. These studies identify a novel pathway in the developing cortex through which glucocorticoids may enhance a metabolic insult, such as hypoxia. KeywordsBcl-2; glucocorticoid receptor; dexamethasone; primary cortical neurons; postnatal; apoptosis Corticosterone, the endogenous glucocorticoid secreted by the rat adrenal gland, binds with high affinity to two different receptors, the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR) (Reagan and McEwen, 1997). MR activation is associated with a neuroprotective phenotype (Almeida et al., 2000), whereas GR activation is implicated in the induction of an endangered neural phenotype (Sapolsky et al., 1986, Reagan andMcEwen, 1997). For example, in the adult, GR activation by the synthetic glucocorticoid Name and address of corresponding author: Robert J. Handa, Colorado State University, Department of Biomedical Sciences, W103 Anatomy, 1617 Campus Delivery, Fort Collins, CO 80523-1617, Phone: (970) Facsimile: (970) Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process er...

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Prenatal stress diminishes neurogenesis in the dentate gyrus of juvenile Rhesus monkeys

Cited by 410 publications

References 72 publications

Developmental brain alterations in 17 year old boys are related to antenatal maternal anxiety

Developmental brain alterations in 17 year old boys are related to antenatal maternal anxiety

Sensory Processing Disorder in a Primate Model: Evidence From a Longitudinal Study of Prenatal Alcohol and Prenatal Stress Effects

Glucocorticoids exacerbate hypoxia-induced expression of the pro-apoptotic gene Bnip3 in the developing cortex

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