Prenatal Effects of Alcohol Abuse in Humans and Laboratory Animals

Streissguth, Ann P.; Martin, Joan C.

doi:10.1007/978-1-4613-3518-4_13

Cited by 18 publications

(16 citation statements)

References 114 publications

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“…Copyright © 2001 National Science Council, ROC and S. Karger AG, Basel In human fetuses, prenatal exposure to alcohol causes a spectrum of effects collectively termed fetal alcohol syndrome. It is commonly found that children of women who were heavy drinkers during pregnancy have mental retardation, hyperactivity, cognitive deficit and behavioral abnormalities [6,41]. These psychological problems induced by prenatal alcohol exposure could be related to central nervous system dysfunction.…”

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confidence: 99%

Alcohol Deters the Outgrowth of Serotonergic Neurons at Midgestation

2001

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We have previously demonstrated that treatment of pregnant C57BL mice from gestation days 8 to 14 with alcohol with 20% ethanol-derived calories (EDC) reduced the number of serotonin (5-HT) neurons and retarded their migration in the fetal brains. In the present study, we obtained similar results with the use of 25% EDC and extended our previous findings by demonstrating that besides the alteration of the number of 5-HT neurons, prenatal alcohol exposure also affects their projecting fibers in their early development. Pregnant C57BL mice were divided into an alcohol-exposed (ALC) group given 25% EDC (4.49%, v/v), a pair-fed group to the ethanol-fed group (PF) and a chow-fed group (Chow). The PF and Chow groups served as controls. Our results showed that in the ALC group, when compared with the control groups, prenatal alcohol exposure with 25% EDC reduced the number of 5-HT-immunoreactive neurons in both the median and dorsal raphe, and the amount of 5-HT-immunoreactive fibers in the medial forebrain bundle (MFB). The diameter of the 5-HT-immunoreactive MFB was also reduced as a result of treatment. No significant differences of the above parameters were found between the PF and Chow groups. The previous and present work confirmed that alcohol reduces the normal formation and growth of 5-HT neurons in the midbrain. Furthermore, the projection of 5-HT fibers, in density as well as in distribution, is reduced in the major trajectory bundle. This may affect the amount of 5-HT fibers available to the forebrain. In light of the importance of the 5-HT system in brain development, alcohol may affect the growth of the forebrain through its effect on 5-HT signaling.

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Alcohol Deters the Outgrowth of Serotonergic Neurons at Midgestation

2001

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“…In the alcohol-exposed fetuses, while unilateral ad renalectomy resulted in a significant in crease in right adrenal weight and in the ratio of right adrenal weight to body weight, it should be noted that for each surgical treatment the right adrenal weight was smaller and the ratio of right adrenal weight to body weight was greater than the values for comparable ad libitum and pair-fed groups. ;V#V s * ae v *V shown to occur in a wide variety of species, including the mouse, rat, dog, pig, and hu man [1][2][3][4][5]. The mechanism by which mater nal alcohol consumption during gestation in fluences fetal growth is not clearly estab lished.…”

Section: Resultsmentioning

confidence: 99%

“…Maternal ingestion of ethanol during ges tation has been shown to retard pre-and postnatal growth of the offspring in a variety of species, including humans [1][2][3][4][5]. In mice, both growth and development are retarded by at least day 12 of gestation [6].…”

Section: Introductionmentioning

confidence: 99%

Compensatory Adrenal Hypertrophy following Unilateral Adrenalectomy of Fetuses of Rats Given Alcohol throughout Gestation

Arishima

Lee²,

Yamamoto³

et al. 1989

Fetal Diagn Ther

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The effect of maternal alcohol consumption on fetal compensatory adrenal hypertrophy following unilateral adrenalectomy was studied in rats. Females were given 20% alcohol in tap water for 4 weeks prior to mating and 30% alcohol in tap water throughout gestation (alcohol), or were pair-fed to the alcohol group (pair-fed) or were fed ad libitum (control). On day 20, fetuses were unilaterally left-adrenalectomized or sham operated. Mothers were sacrificed on day 22 of gestation and right adrenals of adrenalectomized, shamoperated, and unoperated fetuses were removed and weighed. Some adrenals were fixed, sectioned, and stained for histological examination. Adrenalectomized fetuses of all three dietary treatment groups demonstrated compensatory hypertrophy. Adrenals of alcohol exposed fetuses weighed less than those of pair-fed or control fetuses, and the ratio of adrenal weight/body weight was greater, regardless of surgical procedure. Histological sections of right adrenals of left-adrenalectomized fetuses showed larger cells and widened sinusoids, compared to unoperated fetuses in the corresponding dietary treatment groups. These results are consistent with a retardation in adrenal growth and development as a result of alcohol exposure, but show that alcohol consumption throughout gestation does not affect the ability of the adrenals to undergo compensatory hypertrophy following unilateral adrenalectomy.

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“…It is commonly found that children of women who were heavy drinkers during pregnancy exhibit mental retardation, hyperactivity, cognitive deficit and behavioral abnormalities [5,28] . These psychological problems have long been suspected to be related to central nervous system dysfunction.…”

Section: Alcohol and Brain Serotoninmentioning

confidence: 99%

Biomedical Vignette

2001

Journal of Biomedical Science

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Prenatal Effects of Alcohol Abuse in Humans and Laboratory Animals

Cited by 18 publications

References 114 publications

Alcohol Deters the Outgrowth of Serotonergic Neurons at Midgestation

Alcohol Deters the Outgrowth of Serotonergic Neurons at Midgestation

Compensatory Adrenal Hypertrophy following Unilateral Adrenalectomy of Fetuses of Rats Given Alcohol throughout Gestation

Biomedical Vignette

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