Viability and sensorimotor development of mice exposed to prenatal short-term ethanol

Fish, Barbara Schneiderman; Rank, Sara Anne; Wilson, James R.; Collins, Allan C.

doi:10.1016/0091-3057(81)90103-9

Cited by 8 publications

(4 citation statements)

References 37 publications

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“…We selected tests from previously established behavioral screens for neonatal rats (Altman and Sudarshan, 1975; Molina et al, 1987) and mice (Fox, 1965; Schneiderman Fish et al, 1981). All of the tests require the development of both motor and sensory function.…”

Section: Methodsmentioning

confidence: 99%

“…Because gastrulation and neurulation take several days in humans and could be susceptible to a consecutive 2-day exposure, mice were given ethanol twice during either gastrulation on GD7 or neurulation on GD8. The offspring were evaluated for their physical and neurobehavioral development following published reports for mice (Fox, 1965; Schneiderman Fish et al, 1981) and rats (Molina et al, 1987). …”

Section: Introductionmentioning

confidence: 99%

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Low and moderate prenatal ethanol exposures of mice during gastrulation or neurulation delays neurobehavioral development

Schambra

Goldsmith

Nunley

et al. 2015

Neurotoxicology and Teratology

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Human and animal studies show significant delays in neurobehavioral development in offspring after prolonged prenatal exposure to moderate and high ethanol doses resulting in high blood alcohol concentration (BECs). However, none have investigated the effects of lower ethanol doses given acutely during specific developmental time periods. Here, we sought to create a mouse model for modest and circumscribed human drinking during the 3rd and 4th weeks of pregnancy. We acutely treated mice during embryo gastrulation on gestational day (GD) 7 or neurulation on GD8 with a low or moderate ethanol dose given via gavage that resulted in BECs of 107 and 177 mg/dl, respectively. We assessed neonatal physical development (pinnae unfolding, and eye opening); weight gain from postnatal day (PD) 3-65; and neurobehavioral maturation (pivoting, walking, cliff aversion, surface righting, vertical screen grasp, and rope balance) from PD3-17. We used a multiple linear regression model to determine the effects of dose, sex, day of treatment and birth in animals dosed during gastrulation or neurulation, relative to their vehicle controls. We found that ethanol exposure during both time points (GD7 and GD8) resulted in some delays of physical development and significant sensorimotor delays of pivoting, walking, and thick rope balance, as well as additional significant delays in cliff aversion and surface righting after GD8 treatment. We also found that treatment with the low ethanol dose more frequently affected neurobehavioral development of the surviving pups than treatment with the moderate ethanol dose, possibly due to a loss of severely affected offspring. Finally, mice born prematurely were delayed in their physical and sensorimotor development. Importantly, we showed that brief exposure to low dose ethanol, if administered during vulnerable periods of neuroanatomical development, results in significant neurobehavioral delays in neonatal mice. We thus expand concerns about alcohol consumption during the 3rd and 4th week of human pregnancy to include occasional light to moderate drinking.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Low and moderate prenatal ethanol exposures of mice during gastrulation or neurulation delays neurobehavioral development

Schambra

Goldsmith

Nunley

et al. 2015

Neurotoxicology and Teratology

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“…Mostly, they have documented fetal growth restriction following exposure during post‐implantation mouse development (i.e., exposures after gestational day [GD] 6; Sulik et al, 1981; Webster et al, 1983; Downing et al, 2009; Wang et al, 2009). There are some reports of postnatal growth restriction, and these studies suggest that later gestational exposures are critical for this phenotype (Fish et al, 1981; Middaugh et al, 1988; Middaugh and Boggan, 1991, 1995). The few studies that have examined preimplantation or periimplantation gestational exposure (GD 1–6) also observed fetal weight reduction (Padmanabhan and Hameed, 1988; Haycock and Ramsay, 2009), but postnatal growth restriction was not investigated.…”

Section: Introductionmentioning

confidence: 99%

Postnatal growth restriction and gene expression changes in a mouse model of fetal alcohol syndrome

Kaminen‐Ahola

Ahola

Flatscher-Bader

et al. 2010

Birth Defects Research

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Growth restriction, craniofacial dysmorphology, and central nervous system defects are the main diagnostic features of fetal alcohol syndrome. Studies in humans and mice have reported that the growth restriction can be prenatal or postnatal, but the underlying mechanisms remain unknown.We recently described a mouse model of moderate gestational ethanol exposure that produces measurable phenotypes in line with fetal alcohol syndrome (e.g., craniofacial changes and growth restriction in adolescent mice). In this study, we characterize in detail the growth restriction phenotype by measuring body weight at gestational day 16.5, cross-fostering from birth to weaning, and by extending our observations into adulthood. Furthermore, in an attempt to unravel the molecular events contributing to the growth phenotype, we have compared gene expression patterns in the liver and kidney of nonfostered, ethanol-exposed and control mice at postnatal day 28.We find that the ethanol-induced growth phenotype is not detectable prior to birth, but is present at weaning, even in mice that have been cross-fostered to unexposed dams. This finding suggests a postnatal growth restriction phenotype that is not due to deficient postpartum care by dams that drank ethanol, but rather a physiologic result of ethanol exposure in utero. We also find that, despite some catch-up growth after 5 weeks of age, the effect extends into adulthood, which is consistent with longitudinal studies in humans.Genome-wide gene expression analysis revealed interesting ethanol-induced changes in the liver, including genes involved in the metabolism of exogenous and endogenous compounds, iron homeostasis, and lipid metabolism.

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“…Animal offspring of mothers treated with ethanol during the gestation showed a delayed development of body righting (Himwich et al 1977;Lee et al 1980), grasping reflexes (Fish et al 1981), negative geotaxis, air righting and motor balance (Abel & Dintcheff 1978;Demers & Kirouac 1978;Lee et al 1980). In other studies however, no such effects were observed (Caul et al 1979;Da Silva et al 1980;Gallo & Weinberg 1982;Martin et al 1977) or only after combined preand postnatal treatment with ethanol (Shaywitz et al 1979).…”

mentioning

confidence: 99%

Effects of Maternal Ethanol Consumption on the Offspring Sensory‐Motor Development, Ultrasonic Vocalization, Audiogenic Immobility Reaction and Brain Monoamine Synthesis

Hård

Engel

Larsson

et al. 1985

Acta Pharmacologica et Toxicologica

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Female rats were given 16% ethanol solution as the sole liquid during the entire period of gestation. At birth the offspring was removed and reared by foster dams consuming normal tap water. The development of sensory motor behaviour and emotional reactions was delayed by 1–2 days in the prenatally ethanol exposed pups as assessed by tests on body righting, acoustic startle response, air righting, rearing and ultrasonic vocalization. In the open‐field test the normally occurring behavioural difference between the sexes was not found in the prenatally ethanol exposed pups. Both sexes of the ethanol exposed pups behaved like the female controls suggesting deficient masculinization of the ethanol exposed male pups during foetal age. Biochemical analysis of the brains showed a decreased synthesis of serotonin and dopamine.

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Viability and sensorimotor development of mice exposed to prenatal short-term ethanol

Cited by 8 publications

References 37 publications

Low and moderate prenatal ethanol exposures of mice during gastrulation or neurulation delays neurobehavioral development

Low and moderate prenatal ethanol exposures of mice during gastrulation or neurulation delays neurobehavioral development

Postnatal growth restriction and gene expression changes in a mouse model of fetal alcohol syndrome

Effects of Maternal Ethanol Consumption on the Offspring Sensory‐Motor Development, Ultrasonic Vocalization, Audiogenic Immobility Reaction and Brain Monoamine Synthesis

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