Sex differences in learning deficits induced by prenatal stress in juvenile rats

Gué, M.; Bravard, Audrey; Meunier, Johann; Veyrier, Renaud; Gaillet, Sylvie; Récasens, Max; Maurice, Tangui

doi:10.1016/s0166-4328(03)00250-x

Cited by 99 publications

(45 citation statements)

References 48 publications

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“…Our finding that prenatal bystander stress reduced body weight in female rat pups, but not male pups, differs from other research regarding prenatal stress and offspring weight [33,34]. However, because the mechanistic nature of prenatal bystander stress is likely different than direct prenatal stress, differences in outcomes are expected.…”

Section: Discussioncontrasting

confidence: 93%

“…Patin et al [36] also found a reduction in spontaneous locomotion at 2 months of age following repeated prenatal stress. However, research regarding locomotion in juvenile and adult rats demonstrates an increase in activity for offspring exposed to prenatal stress [34,37]. It may be the case that, early in life, prenatally stressed rats are hesitant and unwilling to explore novel environments, but as they age they lose this inhibition and become hyperactive.…”

Section: Discussionmentioning

confidence: 99%

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Prenatal Bystander Stress Alters Brain, Behavior, and the Epigenome of Developing Rat Offspring

et al. 2011

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The prenatal environment, including prenatal stress, has been extensively studied in laboratory animals and humans. However, studies of the prenatal environment usually directly stress pregnant females, but stress may come ‘indirectly’, through stress to a cage-mate. The current study used indirect prenatal bystander stress and investigated the effects on the gross morphology, pre-weaning behavior, and epigenome of rat offspring. Pregnant Long-Evans rats were housed with another female rat that underwent elevated platform stress from gestational days 12 to 16. We found that ultrasonic vocalizations of female cage-mates were disrupted following the stress procedure. After birth, offspring were tested on two behavioral tasks and sacrificed at postnatal day 21 (p21). Frontal cortex and hippocampal tissue was used to measure global DNA methylation and gene expression changes. At p21, bystander-stressed female offspring exhibited increased body weight. Offspring behavior on the negative geotaxis task was altered by prenatal bystander stress, and locomotor behavior was reduced in female offspring. Global DNA methylation increased in the frontal cortex and hippocampus of bystander-stressed offspring. Microarray analysis revealed significant gene expression level changes in 558 different genes, of which only 10 exhibited overlap between males and females or brain areas. These alterations in gene expression were associated with overrepresentation of 36 biological processes and 34 canonical pathways. Prenatal stress thus does not have to be experienced by the mother herself to influence offspring brain development. Furthermore, this type of ‘indirect’ prenatal stress alters offspring DNA methylation patterns, gene expression profiles, and behavior.

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Section: Discussioncontrasting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Prenatal Bystander Stress Alters Brain, Behavior, and the Epigenome of Developing Rat Offspring

et al. 2011

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“…Spontaneous alternation in the Y-maze and performance in the DNMS task depend on the integrity of the mPFC and mainly reflect working memory processes (22,23). Numerous targeted lesion studies in rats and monkeys have shown that working memory performance depends on the mPFC (24), and alcohol dependence produces long-term impairment in PFC function in humans (25,26).…”

Section: Discussionmentioning

confidence: 99%

“…After 5 mo of access to alcohol, 36 rats (12 continuous, 12 intermittent, and 12 naïve rats) were tested after 24 h of abstinence for spontaneous alternation in a Y-maze and after 2 d for anxiety-like behavior in an elevated plus maze. Working memory performance was evaluated with a Y-maze (10 min) as described in the work by Gué et al (23). Anxiety-like behavior was evaluated in a standard elevated plus maze using a videotracking system (Clever Sys).…”

Section: Methodsmentioning

confidence: 99%

Recruitment of medial prefrontal cortex neurons during alcohol withdrawal predicts cognitive impairment and excessive alcohol drinking

George

Sanders

Freiling

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

207

178

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Chronic intermittent access to alcohol leads to the escalation of alcohol intake, similar to binge drinking in humans. Converging lines of evidence suggest that impairment of medial prefrontal cortex (mPFC) cognitive function and overactivation of the central nucleus of the amygdala (CeA) are key factors that lead to excessive drinking in dependence. However, the role of the mPFC and CeA in the escalation of alcohol intake in rats with a history of binge drinking without dependence is currently unknown. To address this issue, we examined FBJ murine osteosarcoma viral oncogene homolog (Fos) expression in the mPFC, CeA, hippocampus, and nucleus accumbens and evaluated working memory and anxiety-like behavior in rats given continuous (24 h/d for 7 d/wk) or intermittent (3 d/wk) access to alcohol (20% vol/vol) using a two-bottle choice paradigm. The results showed that abstinence from alcohol in rats with a history of escalation of alcohol intake specifically recruited GABA and corticotropin-releasing factor (CRF) neurons in the mPFC and produced working memory impairments associated with excessive alcohol drinking during acute (24-72 h) but not protracted (16 -68 d) abstinence. Moreover, abstinence from alcohol was associated with a functional disconnection of the mPFC and CeA but not mPFC and nucleus accumbens. These results show that recruitment of a subset of GABA and CRF neurons in the mPFC during withdrawal and disconnection of the PFC-CeA pathway may be critical for impaired executive control over motivated behavior, suggesting that dysregulation of mPFC interneurons may be an early index of neuroadaptation in alcohol dependence.A lcoholism is a chronic relapsing disorder associated with compulsive drinking, loss of control over intake, and emergence of a negative emotional state during abstinence from the drug (1). Although no known animal model of addiction fully emulates the condition in humans, some models are better suited for the investigation of specific elements of the addiction process in a clinically relevant manner. Recently, an animal model of alcohol binge drinking with good face and predictive validity for what may be considered a transition to alcoholism has been reintroduced (2, 3). Rats given extended (24 h/d) and intermittent (every other day) choice access to ethanol escalate their intake of alcohol over the course of 2-4 wk in a binge-like pattern (2-6), and alcohol drinking using this paradigm was reduced by two drugs approved by the US Food and Drug Administration for the treatment of alcoholism (i.e., naltrexone and acamprosate) (2). Moreover, escalation of alcohol drinking using this model is associated with decreased dopamine levels in the nucleus accumbens after 24 h of abstinence (7), decreased endocannabinoid signaling in the dorsolateral striatum (8), and activation of FBJ murine osteosarcoma viral oncogene homolog B (ΔFosB) in the nucleus accumbens core, dorsolateral striatum, and orbitofrontal cortex.Converging lines of evidence from human and animal studies suggest that impairm...

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“…The rats were confined to the start area for 30 s before testing. The sliding door was then removed, and the rats were allowed to freely explore the rest of the maze for an 8-min trial [26,27]. Numbers of visits to each goal arm and spontaneous alternation performance were recorded by the observer.…”

Section: T Maze For Spontaneous Alternation Performancementioning

confidence: 99%

AMPK activation prevents prenatal stress-induced cognitive impairment: Modulation of mitochondrial content and oxidative stress

Cao

Zheng

et al. 2014

Free Radical Biology and Medicine

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Sex differences in learning deficits induced by prenatal stress in juvenile rats

Cited by 99 publications

References 48 publications

Prenatal Bystander Stress Alters Brain, Behavior, and the Epigenome of Developing Rat Offspring

Prenatal Bystander Stress Alters Brain, Behavior, and the Epigenome of Developing Rat Offspring

Recruitment of medial prefrontal cortex neurons during alcohol withdrawal predicts cognitive impairment and excessive alcohol drinking

AMPK activation prevents prenatal stress-induced cognitive impairment: Modulation of mitochondrial content and oxidative stress

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