Prenatal stress suppresses cell proliferation in the early developing brain

Kawamura, Tatsuyuki; Chen, Jihuan; Takahashi, Taro; Ichitani, Yukio; Nakahara, Daiichiro

doi:10.1097/01.wnr.0000236849.53682.6d

Cited by 61 publications

(48 citation statements)

References 23 publications

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“…Results from animal models of maternal stress support these data and indicate that volumetric abnormalities in prenatally stressed offspring reflect reduced numbers of both neurons and glia, in particular in the hippocampus and amygdala due, in part, to decreased neurogenesis (Coe et al, 2003;Fujioka et al, 2006;Kawamura et al, 2006;Kraszpulski et al, 2006;Lemaire et al, 2000;Rayen et al, 2011). Further, reduced synaptogenesis and hypo-myelination in limbic regions was found in male, but not in female, juvenile rats exposed to maternal stress (Murmu et al, 2006;Xu et al, 2013).…”

Section: Reprogramming In the Prenatally Stressed Brainsupporting

confidence: 70%

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Bronson

Bale

2015

Neuropsychopharmacol

197

180

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Adversity experienced during gestation is a predictor of lifetime neuropsychiatric disease susceptibility. Specifically, maternal stress during pregnancy predisposes offspring to sex-biased neurodevelopmental disorders, including schizophrenia, attention deficit/hyperactivity disorder, and autism spectrum disorders. Animal models have demonstrated disease-relevant endophenotypes in prenatally stressed offspring and have provided unique insight into potential programmatic mechanisms. The placenta has a critical role in the deleterious and sex-specific effects of maternal stress and other fetal exposures on the developing brain. Stress-induced perturbations of the maternal milieu are conveyed to the embryo via the placenta, the maternal-fetal intermediary responsible for maintaining intrauterine homeostasis. Disruption of vital placental functions can have a significant impact on fetal development, including the brain, outcomes that are largely sex-specific. Here we review the novel involvement of the placenta in the transmission of the maternal adverse environment and effects on the developing brain.

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Section: Reprogramming In the Prenatally Stressed Brainsupporting

confidence: 70%

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Bronson

Bale

2015

Neuropsychopharmacol

197

180

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“…There are reports suggesting the possible mechanisms like increased brain corticosterone level (27), altered hypothalamo-pituitary-adrenal (HPA) axis (14), altered neurotransmitters (10) and the altered cellular homeostasis by oxidative damage (10) in brain which in turn involves neuronal death. Though the mechanisms involved in prenatal stress induced neuronal damage is not clearly understood, we hypothesized that the defective antioxidant system in the developing rat brain could be the cause, since brain is particularly vulnerable to oxidative stress due to its high rate of oxygen consumption.…”

Section: Prenatal Stresin Neonatal Sıçan Beyninde Glutatyon Sistemi Ementioning

confidence: 99%

Effect of prenatal stress on expression of glutathione system in neonatal rat brain

Sahu¹,

Madhyastha²,

Rao³

2011

Turkish Neurosurgery

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AIm: Prenatal stress is known to adversely affect the fetal brain development and also neuronal loss. The mechanism(s) associated with prenatal stress induced developmental neurotoxicity remains obscure. Few studies point to the glutathione (GSH) antioxidant system which is an important molecular target for this toxicant. Hence the present study investigates the effect of prenatal stress on glutathione system in neonatal rat brain. mATeRIAL and meTHods: Three to four months old pregnant Wistar rats were subjected to restraint stress during early or late gestational period. The offspring were sacrificed on 40th day and their brain homogenate was subjected to antioxidant studies. The serum corticosterone and adrenal ascorbic acid levels were also estimated from offspring. ResuLTs:The prenatal stress has resulted in an increase in the serum corticosterone and reduced adrenal ascorbic acid levels in neonatal pups. Prenatal stress during early or late gestation life showed reduced glutathione, glutathione reductase (GSSG-Rd) and superoxide dismutase (SOD) activity in offspring brain homogenate.CoNCLusIoN: These data suggest that stress during early or late gestation period affect glutathione system in developing neonatal rat brain, which is associated with elevated serum corticosterone and reduced adrenal ascorbic acid levels.KeywoRds: Prenatal stress, Glutathione, Glutathione reductase, Superoxide dismutase, Antioxidant enzymes ÖZ AmAÇ: Prenatal stresin fetal beyin gelişimi ve ayrıca nöron kaybını olumsuz şekilde etkilediği bilinmektedir. Prenatal stres tarafından indüklenen gelişimsel nörotoksisiteyle ilişkili mekanizma(lar) halen bilinmemektedir. Birkaç çalışma bu toksik madde için önemli bir moleküler hedef olan glutatyon (GSH) antioksidan sistemine işaret etmektedir. Bu nedenle bu çalışma neonatal sıçan beyninde prenatal stresin glutatyon sistemi üzerine etkisini incelemektedir. yÖNTem ve GeReÇLeR: Üç ila dört aylık hamile Wistar sıçanları erken veya geç gestasyonel dönemde zaptetme stresine maruz bırakıldı. Yavrular 40. günde sakrifiye edildi ve beyin homojenatları antioksidan çalışmalara tabi tutuldu. Ayrıca yavrularda serum kortikosteron ve adrenal askorbik asit düzeyleri saptandı.BuLGuLAR: Prenatal stres neonatal sıçanlarda artmış serum kortikosteron ve azalmış adrenal askorbik asit düzeylerine neden oldu. Erken veya geç gestasyonda prenatal stres, yavruların beyin homojenatında azalmış glutatyon, glutatyon redüktaz (GSSG-Rd) ve süperoksit dismutaz (SOD) aktivitesine neden oldu. soNuÇ: Bu veriler erken veya geç gestasyon döneminde stresin gelişen neonatal sıçan beyninde glutatyon sistemini etkilediği ve sonuçta artmış serum kortikosteron ve azalmış adrenal askorbik asit düzeyleriyle ilişkili olduğunu düşündürmektedir.

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“…In rats and non-human primates, the timing of the stressor in the pregnancy has been shown to be important [58][59][60] . A study using rats has shown a 64% increase in the production of corticosterone -a similar hormone to aldosterone in humans -after handling pregnant rats in the last week of gestation and placing them in new, unfamiliar cages 72 .…”

Section: Timing and Severitymentioning

confidence: 99%

“…These regions include the hippocampus [53][54][55][56][57] , amygdala [58][59][60] , corpus callosum 61 , cerebral cortex 62,63 , cerebellum 64,65 and hypothalamus 66,67 . Since morphological changes in the above brain regions have been linked with certain psychological and behavioural problems, it is possible that prenatal stress affects the neurodevelopmental formation of these areas.…”

Section: Microscopic and Macroscopic Changes In The Brainmentioning

confidence: 99%

Os efeitos do estresse na função do eixo hipotalâmico-pituitário-adrenal em indivíduos com esquizofrenia

Guest

Martins-de-Souza²,

Rahmoune

et al. 2012

Arch. Clin. Psychiatry (São Paulo)

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Over the last few decades, evidence has been emerging that the pathogenesis of psychiatric disorders such as schizophrenia can involve perturbations of the hypothalamic-pituitary-adrenal (HPA) axis. Variations in the manifestation of these effects could be related to the differences in clinical symptoms between affected individuals as well as to differences in treatment response. Such effects can also arise from the complex interaction between genes and environmental factors. Here, we review the effects of maternal stress on abnormalities in HPA axis regulation and the development of psychiatric disorders including schizophrenia. Studies in this area may prove critical for increasing our understanding of the multi-dimensional nature of schizophrenia. Further research in this area could ultimately lead to the development of improved diagnostics and novel therapeutic approaches for treating this debilitating psychiatric condition.Guest FL, et al. / Rev Psiq Clín. 2013;40(1):20-7 Keywords: Psychiatric disorders, schizophrenia, HPA axis dysfunction, diagnosis, biomarkers. ResumoNas últimas décadas, têm surgido evidências sugerindo que a patogênese de desordens psiquiátricas, tais como a esquizofrenia, pode envolver perturbações no eixo hipotalâmico-pituitário-adrenal (HPA). Variações na manifestação desses efeitos poderiam estar relacionadas a diferenças em sintomas clínicos entre os indivíduos afetados, assim como a diferenças na resposta ao tratamento. Tais efeitos podem também ser originados de complexas interações entre genes e fatores ambientais. Aqui, revisamos os efeitos do estresse maternal em anormalidades na regulação do eixo HPA e desenvolvimento de desordens psiquiátricas, incluindo a esquizofrenia. Estudos nessa área podem gerar o aumento do nosso entendimento da natureza multidimensional da esquizofrenia. Posterior pesquisa nesse campo poderia, em última instância, levar ao desenvolvimento de melhores diagnósticos e novas abordagens terapêuticas para essa debilitante condição psiquiátrica.Guest FL, et al. / Rev Psiq Clín. 2013;40(1):20-7 Palavras-chave: Desordens psiquiátricas, esquizofrenia, disfunção do eixo HPA, diagnóstico, biomarcadores.

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Prenatal stress suppresses cell proliferation in the early developing brain

Cited by 61 publications

References 23 publications

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Effect of prenatal stress on expression of glutathione system in neonatal rat brain

Os efeitos do estresse na função do eixo hipotalâmico-pituitário-adrenal em indivíduos com esquizofrenia

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