Prenatal stress causes gender‐dependent neuronal loss and oxidative stress in rat hippocampus

Zhu, Zhongliang; Li, Xia; Chen, Weina; Zhao, Yan; Li, Hui; Cai, Qing-Qing; Jia, Na; Bai, Zhuanli; Liu, Jiankang

doi:10.1002/jnr.20338

Cited by 104 publications

(104 citation statements)

References 37 publications

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“…acid level, our findings were consistent with earlier reports (12,15,30). Zhu et al (2004) investigated the effect of prenatal stress during middle and late gestation on neuronal loss and oxidative stress.…”

Section: Sahu S Et Al: Effect Of Prenatal Stress On Rat Brainsupporting

confidence: 93%

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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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Section: Sahu S Et Al: Effect Of Prenatal Stress On Rat Brainsupporting

confidence: 93%

“…Zhu et al (2004) investigated the effect of prenatal stress during middle and late gestation on neuronal loss and oxidative stress. They measured free intracellular Ca 2+ and intracellular reactive oxygen species formation.…”

Section: Sahu S Et Al: Effect Of Prenatal Stress On Rat Brainmentioning

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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“…In AD and after hypoxic/ischemic insults, CA1 region typically demonstrates profound vulnerability to neuronal cell death (SchmidtKastner and Freund, 1991;West et al, 1994). Regional susceptibility similar to that seen in our experiments has been reported with human immunodeficiency virus transactivating protein TAT, prenatal stress, and okadaic acid, in which pyramidal cells in the CA3 region and granule cells in DG are more sensitive compared with pyramidal cells in CA1 (Runden et al, 1998;Maragos et al, 2003;Zhu et al, 2004). The mechanism of okadaic acid toxicity is likely attributable to sustained activation of the mitogen-activated protein kinase (MAP kinase) pathway (Runden et al, 1998).…”

Section: Mechanisms Of Cell Deathsupporting

confidence: 83%

Tau Aggregation and Progressive Neuronal Degeneration in the Absence of Changes in Spine Density and Morphology after Targeted Expression of Alzheimer's Disease-Relevant Tau Constructs in Organotypic Hippocampal Slices

Shahani¹,

Subramaniam²,

Wolf³

et al. 2006

J. Neurosci.

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Alzheimer's disease (AD) is characterized by progressive loss of neurons in selected brain regions, extracellular accumulations of amyloid ␤, and intracellular fibrils containing hyperphosphorylated tau. Tau mutations in familial tauopathies confirmed a central role of tau pathology; however, the role of tau alteration and the sequence of tau-dependent neurodegeneration in AD remain elusive. Using Sindbis virus-mediated expression of AD-relevant tau constructs in hippocampal slices, we show that disease-like tau modifications affect tau phosphorylation at selected sites, induce Alz50/MC1-reactive pathological tau conformation, cause accumulation of insoluble tau, and induce region-specific neurodegeneration. Live imaging demonstrates that tau-dependent degeneration is associated with the development of a "ballooned" phenotype, a distinct feature of cell death. Spine density and morphology is not altered as judged from algorithmbased evaluation of dendritic spines, suggesting that synaptic integrity is remarkably stable against tau-dependent degeneration. The data provide evidence that tau-induced cell death involves apoptotic as well as nonapoptotic mechanisms. Furthermore, they demonstrate that targeted expression of tau in hippocampal slices provides a novel model to analyze tau modification and spatiotemporal dynamics of tau-dependent neurodegeneration in an authentic CNS environment.

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“…Female offspring of both prenatal treatment groups failed to show intact object-in-place memory (Howland et al, 2012). These sex-specific deficits contrast with those seen by others (Gue et al, 2004;Zhu et al, 2004) who demonstrated deficits that are more pronounced in female than male offspring using different prenatally-induced stressors.…”

Section: Learning and Memorycontrasting

confidence: 65%

Sex effects on neurodevelopmental outcomes of innate immune activation during prenatal and neonatal life

Rana

Aavani

Pittman

2012

Hormones and Behavior

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Humans are exposed to potentially harmful agents (bacteria, viruses, toxins) throughout our lifespan; the consequences of such exposure can alter central nervous system development. Exposure to immunogens during pregnancy increases the risk of developing neurological disorders such as schizophrenia and autism. Further, sex hormones, such as estrogen, have strong modulatory effects on immune function and have also been implicated in the development of neuropathologies (e.g., schizophrenia and depression). Similarly, animal studies have demonstrated that immunogen exposure in utero or during the neonatal period, at a time when the brain is undergoing maturation, can induce changes in learning and memory, as well as dopaminemediated behaviors in a sex-specific manner. Literature that covers the effects of immunogens on innate immune activation and ultimately the development of the adult brain and behavior is riddled with contradictory findings, and the addition of sex as a factor only adds to the complexity. This review provides evidence that innate immune activation during critical periods of development may have effects on the adult brain in a sex-specific manner. Issues regarding sex bias in research as well as variability in animal models of immune function are discussed.

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Prenatal stress causes gender‐dependent neuronal loss and oxidative stress in rat hippocampus

Cited by 104 publications

References 37 publications

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

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

Tau Aggregation and Progressive Neuronal Degeneration in the Absence of Changes in Spine Density and Morphology after Targeted Expression of Alzheimer's Disease-Relevant Tau Constructs in Organotypic Hippocampal Slices

Sex effects on neurodevelopmental outcomes of innate immune activation during prenatal and neonatal life

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