The fetal alcohol syndrome: A review and assessment of the syndrome and its neurological sequelae

Colangelo, Wendy; Jones, D.G.

doi:10.1016/0301-0082(82)90009-0

Cited by 65 publications

(19 citation statements)

References 183 publications

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“…Previous studies have similarly shown that prenatal ethanol exposure differentially affects HPA function in males and fe-ma~es.6,. '0.~ 1,13,45,49 Although E males and females may both exhibit increased HPA responsiveness, it appears that the nature and intensity of the stressor, as well as the time course and hormonal endpoint measured may all influence the outcome observed and may reveal differential effects in males and females.13 Rats have been shown to exhibit sexual dimorphism of the HPA axis. Typically, females have heavier adrenals glands, higher ACTH, CORT, and CBG levels, and greater diurnal variations in CORT levels than males.47,50-52 These sex differences are due to both organizational and activational effects of the sex hormones.47S2-54 These sex differences in responsiveness observed in our study may be due to interactions of prenatal ethanol, exposure to stressors, and the naturally occurring sexual dimorphism of HPA activity.…”

Section: Discussionmentioning

confidence: 99%

Effects of Prenatal Ethanol Exposure on Hypothalamic‐Pituitary‐Adrenal Responses to Chronic Cold Stress in Rats

Kim

Giberson

et al. 1999

Alcoholism Clin & Exp Res

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Animals prenatally exposed to ethanol typically exhibit hypothalamic-pituitary-adrenal (HPA) hyperresponsiveness to stressors. In contrast to previous studies that have investigated effects of prenatal ethanol exposure on HPA responses to acute or intermittent stressors, our study investigated HPA responses to a chronic continuous stressor, cold stress (4 degrees C for 0, 1, or 3 days). We tested the hypothesis that prenatal ethanol exposure would result in increased plasma corticosterone (CORT) and adrenocorticotropin (ACTH) responses and increased peptide [corticotropin-releasing factor and vasopressin] mRNA levels in the paraventricular nucleus (PVN) of the hypothalamus compared to that in control animals. In addition, CORT and ACTH responses were measured after exposure to an acute stressor (i.p. isotonic saline injection), superimposed during chronic cold exposure, to examine possible sensitization of the HPA response to the acute stress. Thus, blood samples were collected at the end of each of the three periods of cold exposure, either before (0 min) or 15 min after acute stress. The subjects were adult male and female Sprague-Dawley rat offspring from prenatal ethanol (E), pair-fed (PF), and ad libitum-fed control (C) treatment groups. Exposure to cold stress resulted in significant body weight loss in E males at 1 day and in both males and females of all prenatal treatment groups by 3 days of cold stress. Males in all prenatal groups also exhibited significant increases in adrenal weight:body weight ratios. Cold stress alone (0 min condition) increased CORT levels in E males and overall ACTH levels in E males and females compared to controls. ACTH levels were also higher overall in E compared to control males after acute stress (15 min condition). Sensitization of the CORT response to acute stress was observed in males but not females across all prenatal treatment groups. Corticotropin-releasing factor and vasopressin mRNA levels in the PVN were not significantly affected by prenatal treatment or chronic cold stress in either males or females. In contrast, both males and females displayed increases in PVN thyrotropin-releasing hormone (TRH) mRNA levels after cold stress. These data support and extend previous work demonstrating differential effects of prenatal ethanol exposure on HPA responsiveness of male and female offspring, and suggest that E males may be more vulnerable to the effects of chronic cold stress than E females.

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Section: Discussionmentioning

confidence: 99%

Effects of Prenatal Ethanol Exposure on Hypothalamic‐Pituitary‐Adrenal Responses to Chronic Cold Stress in Rats

Kim

Giberson

et al. 1999

Alcoholism Clin & Exp Res

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“…The fetal alcohol syndrome (FAS) is a triad consisting of CNS dysfunction, intrauterine growth deficiency, and distinctive facial dysmorphism; less often there are anomalies of the heart, skeleton, urogenital organs, skin and muscles [128,129]. Symptoms include mental retardation, hypotonia, poor coordination, hyperactivity, and behavioral problems.…”

Section: Ethanol’s Effects On the Fetusmentioning

confidence: 99%

Ethanol and Cognition: Indirect Effects, Neurotoxicity and Neuroprotection: A Review

Brust

2010

IJERPH

209

127

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Ethanol affects cognition in a number of ways. Indirect effects include intoxication, withdrawal, brain trauma, central nervous system infection, hypoglycemia, hepatic failure, and Marchiafava-Bignami disease. Nutritional deficiency can cause pellagra and Wernicke-Korsakoff disorder. Additionally, ethanol is a direct neurotoxin and in sufficient dosage can cause lasting dementia. However, ethanol also has neuroprotectant properties and in low-to-moderate dosage reduces the risk of dementia, including Alzheimer type. In fetuses ethanol is teratogenic, and whether there exists a safe dose during pregnancy is uncertain and controversial.

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“…Prenatal ethanol exposure has been reported to cause a delay in the maturation of the nervous system (Clarren and Smith, 1978;Colangelo and Jones, 1982). Our data suggest that this ethanol-induced delay in neural development reported by many investigators is a result of a general effect on the process of transcription, reflected in the pattern of appearance of various mRNAs.…”

Section: Discussionmentioning

confidence: 44%

“…In the case of ethanol, prenatal exposure may lead to the condition known as fetal alcohol syndrome, characterized by intrauterine growth retardation, microcephaly, craniofacia1 and eye abnormalities, and mental deficiency (Colangelo and Jones, 1982). Ethanol may exert its effects on neural development a t various levels, and little is presently known concerning the specific teratological mechanism(s) involved (West, 1986).…”

Section: Introductionmentioning

confidence: 99%

Effect of prenatal ethanol exposure on postnatal neural gene expression in the rat

Naus

Bechberger

1991

Dev. Genet.

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To examine the effects of ethanol exposure on neural development, pregnant rats were fed a liquid diet in which 37.5% of the total caloric content was ethanol-derived. The developmental appearance of the messenger RNAs coding for preprosomatostatin, glial fibrillary acidic protein, and proteolipid protein was examined by Northern blotting of total cellular RNA obtained from forebrain and hindbrain at various times after birth. In general, there was a delay in the developmental pattern of appearance of these mRNAs which was most noticeable at the early postnatal times. These results suggest that the previously reported delay in neural maturation is reflected at the level of the gene expression.

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The fetal alcohol syndrome: A review and assessment of the syndrome and its neurological sequelae

Cited by 65 publications

References 183 publications

Effects of Prenatal Ethanol Exposure on Hypothalamic‐Pituitary‐Adrenal Responses to Chronic Cold Stress in Rats

Effects of Prenatal Ethanol Exposure on Hypothalamic‐Pituitary‐Adrenal Responses to Chronic Cold Stress in Rats

Ethanol and Cognition: Indirect Effects, Neurotoxicity and Neuroprotection: A Review

Effect of prenatal ethanol exposure on postnatal neural gene expression in the rat

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