The Effects of Prenatal Alcohol Exposure on Behavior: Rodent and Primate Studies

Schneider, Mary L.; Moore, Colleen F.; Adkins, Miriam M.

doi:10.1007/s11065-011-9168-8

Cited by 124 publications

(112 citation statements)

References 154 publications

(198 reference statements)

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“…Although many disorders of genetic and/or environmental origin are associated with developmental delays in cognitive function (Cornish et al 2004;Sagvolden et al 2005;Riley et al 2011), most current animal models typically do not assess cognitive function until adulthood or perhaps at one or two isolated developmental stages. For instance, fetal alcohol exposure is consistently found to produce widespread effects on learning and memory in rodents that are present during adolescence and adulthood (Berman and Hannigan 2000;Schneider et al 2011), but relatively little is known regarding the developmental onset of these effects in younger animals (e.g., Blanchard et al 1987;Wigal et al 1988;Kirstein et al 1997). Our finding that the ability to form context-shock associations is delayed by up to 2 d in fetal alcohol-exposed mice demonstrates that a detailed ontogenetic timeline of contextual fear memory can be used as a template to compare normal vs. abnormal cognitive development.…”

Section: Learning and Memorymentioning

confidence: 99%

“…Pinpointing the precise age when animals begin to form memories of aversive events can be valuable for understanding the onset of anxiety and mood disorders stemming from maladaptive early life experience (Pine 2009;Bale et al 2010;Marco et al 2011) and for detecting early cognitive impairment in models of autism, attention deficit/hyperactivity disorder, and fetal alcohol syndrome (Schneider et al 2011;Kaffman and Krystal 2012). During infancy and adolescence, the progressive growth and refinement of neural circuitry supporting sensation and perception (Bourne 2010;Froemke and Jones 2011), cognition (Benes et al 2000;Dumas 2005), and emotion (Braun 2011) gradually enables young rodents to begin learning about their surroundings.…”

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Ontogeny of contextual fear memory formation, specificity, and persistence in mice

et al. 2012

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Pinpointing the precise age when young animals begin to form memories of aversive events is valuable for understanding the onset of anxiety and mood disorders and for detecting early cognitive impairment in models of childhood-onset disorders. Although these disorders are most commonly modeled in mice, we know little regarding the development of learning and memory in this species because most previous studies have been restricted to rats. Therefore, in the present study, we constructed an ontogenetic timeline of contextual fear memory ranging from infancy to adulthood in mice. We found that the ability of mice to form long-term context-shock associations emerged 13 -14 d of age, which is several days earlier than previously reported for rats. Although the ability to form contextual fear memories remained stable from infancy into adulthood, infant mice had shorter-lasting memories than adolescent and adult mice. Furthermore, we found that mice subjected to fetal alcohol exposure showed a delay in the developmental emergence of contextual fear memory, illustrating the utility of this ontogenetic approach in detecting developmental delays in cognitive function stemming from maladaptive early life experience.

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Section: Learning and Memorymentioning

confidence: 99%

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confidence: 99%

Ontogeny of contextual fear memory formation, specificity, and persistence in mice

et al. 2012

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Neurobehavioral evaluation of mouse newborns exposed prenatally to low-dose bisphenol A

et al. 2014

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INTRODUCTIONStudies with rodents show that prenatal exposure to some neurotoxicants adversely affects neonatal orientation, attention and motor maturity, as well as activity level, executive function, response inhibition and sensory processing later in life (Schneider et al., 2011). Although there have been a vast number of animal toxicological studies carried out on pregnant animals including embryos/fetuses and mature animals, there is a paucity of reports on animal toxicology studies utilizing newborn animals a few days after birth. To evaluate the neurotoxic effects of chemicals on newborns in rodents, we very recently developed a mouse newborn neurobehavioral testing method; it involves quantitative determination of a newborn animal's activity automatically using the tare function of an analytical balance. We have demonstrated that developmentally 10 mg/kg methylnitrosourea-treated ICR mice showed increases in motor behavior including crawling, pivoting, righting or tremors when estimating this activity by this testing method on postnatal day 1 (Nagao et al., 2013).Bisphenol A (BPA) is one of the environmental endocrine disruptors released by plastics and resin known to interfere with hormonal responses. During fetal life, the intrauterine environment is critical for normal development, and even small changes in the levels of hormones may lead to changes in brain histology and function, and consequently in behavior. Nuclear estrogen receptor binding assays indicate that BPA has at least a 10,000-fold lower affinity for the two estrogen nuclear receptors than 17β-estradiol. In isolation, these results would suggest that BPA at environmentally relevant levels of exposure would not pose a public health problem (Zoeller et al., 2012). However, low doses of BPA administered perinatally can modify explorative behavior and anxiety in rat (Fujimoto et al., 2013). It has been shown that perinatal BPA exposure disrupted sexually dimorphic behavior in the postnatal developmental period and in adult mice, when evaluated by the elevated plus maze test and the open field test (Gioiosa et al., 2013;Nakamura et al., 2012). In addition, mice treated with BPA prenatally were hyperactive, like attention-deficit hyperactivity disorder (ADHD), in these behavioral tests. The mode of action underlying these effects is unclear. Recently, we demonstrated that histological changes of the cortical plate were found in mouse fetuses exposed to a low dose of BPA (Komada et al., 2012), and that prenatally BPA-treated mice showed hyperplasia of layer 6b and abnormal neuronal distribution in the neocortex of newborn (our unpubNeurobehavioral evaluation of mouse newborns exposed prenatally to low-dose bisphenol A Kusumoto-cho, Chikusa-ku, Nagoya, Aichi 464-8650, Japan (Received December 18, 2013; Accepted January 16, 2014) ABSTRACT -There have been few neurobehavioral toxicology studies on newborn animals. Thus, we developed a mouse newborn behavioral testing method for evaluating the risk of neurotoxicity of environmental toxicants, ...

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“…Animal models using higher-order primates (rhesus monkeys) mirror those conducted with rodents and have demonstrated that, under conditions of prenatal stress and alcohol exposure, outcomes include lower birth weights, increased stereotypical behavior, reduced attention span, decreased exploration and play behavior, and increased activity levels early in life [26]. Importantly, prenatally stressed adolescent monkeys with PAE exhibit an increase in alcohol preference over time, suggesting a vulnerability to SUDs similar to that found in humans.…”

Section: Animal Models Of Mental Health Problemsmentioning

confidence: 99%

Mental Health Outcomes Associated with Prenatal Alcohol Exposure: Genetic and Environmental Factors

O’Connor¹

2014

Curr Dev Disord Rep

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Overwhelming evidence on the impact of maternal alcohol consumption during pregnancy has prompted increased attention to the link between prenatal alcohol exposure (PAE) and a constellation of developmental disabilities, which are characterized by physical, cognitive, and behavioral impairments. Importantly, individuals with PAE are particularly vulnerable to mental health problems. This review summarizes the current literature on the underlying mechanisms of PAE vulnerability, including epigenetic, genetic, and environmental risk factors that predispose individuals with PAE to psychiatric illness. The studies cited are from animal and human research and include a developmental perspective. Research on the mental health problems suffered by individuals with fetal alcohol spectrum disorders (FASDs) throughout development highlights the need for training of mental health professionals in the identification and the provision of specific treatments to address the unique features of this developmental disability.

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The Effects of Prenatal Alcohol Exposure on Behavior: Rodent and Primate Studies

Cited by 124 publications

References 154 publications

Ontogeny of contextual fear memory formation, specificity, and persistence in mice

Ontogeny of contextual fear memory formation, specificity, and persistence in mice

Neurobehavioral evaluation of mouse newborns exposed prenatally to low-dose bisphenol A

Mental Health Outcomes Associated with Prenatal Alcohol Exposure: Genetic and Environmental Factors

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