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Reductions in the plating efficiency of the fetal neural precursor cells following maternal alcohol consumption
Author(s) -
Kennedy L.A.,
Elliot M.J.,
Laverty W.H.
Publication year - 1984
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/0736-5748(84)90045-5
Subject(s) - fetus , neocortex , precursor cell , neural tube , biology , morphogenesis , gestation , fetal alcohol syndrome , endocrinology , neural stem cell , mitosis , medicine , andrology , pregnancy , in vitro , alcohol , microbiology and biotechnology , embryo , neuroscience , biochemistry , stem cell , genetics , gene
Maternal alcohol abuse has been associated with reduced neural cell number and abnormal cell differentiation and organization in many regions of the developing mammalian brain. Experiments were conducted to determine whether changes in the neural precursor cells could be detected in primary culture following maternal alcohol consumption during the early proliferative period of the fetal brain growth spurt. Alcohol was administered to pregnant mice in the drinking water from days 11 to 19 of gestation. There was no alcohol‐related increase in the incidence of fetal mortality or malformation, but fetal body and brain weights were reduced. When disaggregated cells from the day 19 fetal neopallium were grown in culture, there was a reduction in the number of astroglial colonies yielded in 42% of alcohol‐exposed brains. This effect was expressed as a reduction in the absolute plating efficiency (APE) of the neural precursor cells. The APE was reduced as much as 80% in severely affected brains. There was no alcoholrelated difference in the in vitro morphogenesis of the astroglial colonies. Observations of the proliferative neural cells in situ suggest that there is an impaired recruitment of all neural cell types, but that the reduced APE reflects primarily a proportionate increase in the number of immature neurons among the cells obtained from the fetal neopallium. It appears that a prolongation of mitosis may be resulting in a general developmental delay in the fetal neocortex.