Growth patterns of rat body, brain, and cerebellum in fetal alcohol syndrome

Nathaniel, E.J.H.; Nathaniel, Doris R.; Mohamed, Seham M.; Nahnybida, L.; Nathaniel, L.

doi:10.1016/0014-4886(86)90180-9

Cited by 44 publications

(13 citation statements)

References 24 publications

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“…Our finding that prenatal exposure to ethanol reduced the weight of offspring is consistent with previously published reports (Hannigan, 1995, Nathaniel et al, 1986). However, the deficits in weight we observed did not appear to emerge until at least weaning (PD21), and were gone by adulthood (PD94).…”

Section: Discussionsupporting

confidence: 93%

“…However, the deficits in weight we observed did not appear to emerge until at least weaning (PD21), and were gone by adulthood (PD94). A number of studies have also indicated that brain weights are reduced in the offspring of dams exposed to ethanol during gestation (Nathaniel et al, 1986). Although brain weights following prenatal exposure to binge-like ethanol intake did not differ at birth, it is unclear whether any such deficits might have emerged as the pups matured.…”

Section: Discussionmentioning

confidence: 99%

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Using drinking in the dark to model prenatal binge‐like exposure to ethanol in C57BL/6J mice

Boehm

Moore

Walsh

et al. 2008

Developmental Psychobiology

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Animal models of prenatal ethanol exposure are necessary to more fully understand the effects of ethanol on the developing embryo/fetus. However, most models employ procedures that may produce additional maternal stress beyond that produced by ethanol alone. We employed a daily limited-access ethanol intake model called Drinking in the Dark (DID) to assess the effects of voluntary maternal binge-like ethanol intake on the developing mouse. Evidence suggests that binge exposure may be particularly harmful to the embryo/fetus, perhaps due to the relatively higher blood ethanol concentrations achieved. Pregnant females had mean daily ethanol intakes ranging from 4.2-6.4 g/kg ethanol over gestation, producing blood ethanol concentrations ranging from 115-182 mg/dl. This level of ethanol intake produced behavioral alterations among adolescent offspring that disappeared by adulthood, including altered sensitivity to ethanol’s hypnotic actions. The DID model may provide a useful tool for studying the effects of prenatal ethanol exposure in mice.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Using drinking in the dark to model prenatal binge‐like exposure to ethanol in C57BL/6J mice

Boehm

Moore

Walsh

et al. 2008

Developmental Psychobiology

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“…Investigations in rats have provided, in some cases, support and, in some cases, no support for the hypothesis that thyroid system dysfunction is involved in mediating ARBDs. In rats, maternal ethanol exposure during gestation results in reduced T 4 in newborn rats (Hannigan and Bellisario, 1990;Nathaniel et al, 1986), reduced maternal T 4 during pregnancy, decreased T 3 and T 4 in pups at birth (Portolés et al, 1988), reduced thyroid mass in the late-term fetus (Yamamoto et al, 1989), and altered messenger RNA expression of brain thyroid hormone receptors (Scott et al, 1998). However, Lee and Wakabayashi (1986) did not detect changes in fetal T 4 levels measured at term after maternal ethanol exposure.…”

Section: Discussionmentioning

confidence: 94%

Fetal and Maternal Thyroid Hormone Responses to Ethanol Exposure During the Third Trimester Equivalent of Gestation in Sheep

Cudd

Chen

West

2002

Alcoholism Clin & Exp Res

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“…The animal models have been useful in clarifying the mechanism of ethanol teratogenicity . Ethanol-induced alterations in the development of neurons and glia underlie the behavioral problems associated with FAS (e .g ., Weinberg et al, 1979a, b ;Henderson et al ., 1981 ;Kennedy, 1984 ;Miller 1986Miller , 1992aNathaniel et al ., 1986 ;Sanchis et al ., 1987 ;Druse, 1992) . Many of the developmental defects lead to permanent morphological and functional abnormalities (Pentney and Miller, 1992 ;Ward and West, 1992) .…”

mentioning

confidence: 99%

Iron Regulation in the Developing Rat Brain: Effect of In Utero Ethanol Exposure

Miller

Roskams

Connor

1995

Journal of Neurochemistry

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Fetal alcohol syndrome produces defects that parallel abnormalities associated with early iron deficiency. Hence, we examined the effects of prenatal exposure to ethanol on iron, transferrin, and ferritin concentrations. The subjects were the offspring of pregnant rats fed an ethanol‐containing diet (Et), pair‐fed an isocaloric control diet (Ct), or fed chow and water. The amounts of iron, transferrin, and ferritin were assessed in three CNS regions (cerebral cortex, subcortical forebrain, and brain‐stem). In all three segments of the control rats, iron, transferrin, and ferritin levels decreased during the first 2 postnatal weeks, reached a minimum during week 3, and then rose to adult levels. This pattern was delayed by ethanol treatment, e.g., the minimal concentrations in iron, transferrin, and ferritin in the Et‐treated rats were achieved later (3 days, 7 days, and 2 weeks, respectively) than they were in the Ct‐treated rats. Ethanol‐induced alterations in iron homeostasis persisted into adulthood; iron concentration was reduced, transferrin concentration was unaffected, and ferritin concentration was increased. The net result was that the timely delivery and bioavailability of iron were compromised by ethanol exposure. The defects in iron regulation are permanent and may underlie ethanol‐induced abnormalities in iron‐dependent growth processes such as myelination.

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Growth patterns of rat body, brain, and cerebellum in fetal alcohol syndrome

Cited by 44 publications

References 24 publications

Using drinking in the dark to model prenatal binge‐like exposure to ethanol in C57BL/6J mice

Using drinking in the dark to model prenatal binge‐like exposure to ethanol in C57BL/6J mice

Fetal and Maternal Thyroid Hormone Responses to Ethanol Exposure During the Third Trimester Equivalent of Gestation in Sheep

Iron Regulation in the Developing Rat Brain: Effect of In Utero Ethanol Exposure

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