Environmental Health Factors and Sexually Dimorphic Differences in Behavioral Disruptions

Rosenfeld, Cheryl S.; Trainor, Brian C.

doi:10.1007/s40572-014-0027-7

Cited by 28 publications

(24 citation statements)

References 164 publications

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“…Although women are not aware of their exposures, women may systematically rate boys and girls differently which can exert unknown and systematic biases on results. There is significant investment in animal models to evaluate potential mechanisms that may mediate effects (Rosenfeld and Trainor, 2014, De Felice et al, 2015). …”

Section: Fetal Sex As a Moderator Of Prenatal Exposuresmentioning

confidence: 99%

The gestational foundation of sex differences in development and vulnerability

2017

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Despite long-standing interest in the role of sex on human development, the functional consequences of fetal sex on early development are not well understood. Here we explore the gestational origins of sex as a moderator of development. In accordance with the focus of this special issue, we examine evidence for a sex differential in vulnerability to prenatal and perinatal risks. Exposures evaluated include those present in the external environment (e.g., lead, pesticides), those introduced by maternal behaviors (e.g., alcohol, opioid use), and those resulting from an adverse intrauterine environment (e.g., preterm birth). We also provide current knowledge on the degree to which sex differences in fetal neurobehavioral development (i.e., cardiac and motor patterns) are present prior to birth. Also considered are contemporaneous and persistent sex of fetus effects on the pregnant woman. Converging evidence confirms that infant and early childhood developmental outcomes of male fetuses exposed to prenatal and perinatal adversities are more highly impaired than those of female fetuses. In certain circumstances, male fetuses are both more frequently exposed to early adversities and more affected by them when exposed than are female fetuses. The mechanisms through which biological sex imparts vulnerability or protection on the developing nervous system are largely unknown. We consider models that implicate variation in maturation, placental functioning, and the neuroendocrine milieu as potential contributors. Many studies use sex as a control variable, some analyze and report main effects for sex, but those that report interaction terms for sex are scare. As a result, the true scope of sex differences in vulnerability is unknown.

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Section: Fetal Sex As a Moderator Of Prenatal Exposuresmentioning

confidence: 99%

The gestational foundation of sex differences in development and vulnerability

2017

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“…However, a very robust and consistent finding across this recent literature on several mammalian species, including humans, is that whenever both sexes were examined, sex is a fundamental variable in accounting for BPA effects on behavior. Many studies demonstrate that BPA exposure during development is able to disrupt sexually dimorphic behaviors in different species (reviewed in [5,35,36]).…”

Section: Behaviormentioning

confidence: 99%

“…Disruption of hormonally controlled, sexual differentiation of the brain may increase vulnerability for disturbance of these, or other, sexually dimorphic functions. Development of psychological disorders with sex-biased prevalence rates may be associated with the disruption of developmental trajectory and/or maturation of the sexually dimorphic brain [36,39]. According to the ‘developmental origins of health and disease (DOHaD)’ hypothesis, many adult disorders have roots early in life, and environmental factors during perinatal development can dramatically shape the individual’s risk for later diseases [43].…”

Section: Sexmentioning

confidence: 99%

Perinatal exposure to endocrine disruptors: sex, timing and behavioral endpoints

Palanza

Nagel

Parmigiani

et al. 2016

Current Opinion in Behavioral Sciences

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Of the approximately 85,000 chemicals in use, 1000 have been identified as having the ability to disrupt normal endocrine function. Exposure to endocrine disrupting chemicals (EDCs) during critical period in brain differentiation (prenatal and neonatal life) via the mother can alter the course of the development of sexually dimorphic behaviors. Bisphenol A (BPA) is a very high volume chemical used in plastic, resins and other products, and virtually everyone examined has detectable BPA. BPA has estrogenic activity and is one of the most studied EDCs. We review evidence from studies in rodents using dose levels relevant to human exposure. BPA alters behavior and eliminates or in some cases reverses sexually dimorphic behaviors observed in unexposed animals.

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“…There is growing evidence that exposure to EDCs such as BPA early in life can interact with stressors experienced later in life. This idea has been conceptualised as the “two hit” hypothesis, which poses that a combination of external hits can produce a phenotype that is greater than the sum of their individual effects . As a first step towards testing this hypothesis, we examined the individual effects of developmental BPA exposure (or ethinyl oestradiol: EE, positive oestrogen control for BPA studies) or social defeat experienced at adulthood on DNMT gene expression.…”

Section: Introductionmentioning

confidence: 99%

Exposure to extrinsic stressors, social defeat or bisphenol A, eliminates sex differences in DNA methyltransferase expression in the amygdala

Wright

Johnson

Hao

et al. 2017

J Neuroendocrinology

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Chemical and psychological stressors can exert long lasting changes in brain function and behavior. Changes in DNA methylation have been shown to be an important mechanism mediating long lasting changes in neural function and behavior, especially for anxiety-like or stress responses. Here we examined the effects of either a social or chemical stressor on DNA methyltransferase (DNMT) gene expression in the amygdala, an important brain region modulating stress responses and anxiety. In adult California mice (Peromyscus californicus) that were naïve to social defeat, females had higher levels of Dnmt1 expression in punch samples of the central amygdala (CeA) than males. In addition, social defeat stress reduced Dnmt1 and Dnmt3a expression in the CeA of females but not males. A second study using more anatomically specific punch samples replicated these effects for Dnmt1. Perinatal exposure, spanning from periconception through lactation, to bisphenol A or ethinyl estradiol (estrogens in birth control pills) also abolished sex differences in Dnmt1 expression in the CeA but not basolateral amygdala. These findings identify a robust sex difference in Dnmt1 expression in the CeA that is sensitive to both psychological and chemical stressors. Our results suggest that future studies should examine the impact of psychological and chemical stressors on DNA methylation in the CeA and that Dnmt1 may have an underappreciated role in plasticity in behavior.

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Environmental Health Factors and Sexually Dimorphic Differences in Behavioral Disruptions

Cited by 28 publications

References 164 publications

The gestational foundation of sex differences in development and vulnerability

The gestational foundation of sex differences in development and vulnerability

Perinatal exposure to endocrine disruptors: sex, timing and behavioral endpoints

Exposure to extrinsic stressors, social defeat or bisphenol A, eliminates sex differences in DNA methyltransferase expression in the amygdala

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