EFFECTS OF COMBINED PRENATAL AND POSTNATAL ETHANOL EXPOSURE (3 TRIMESTER EQUIVALENCY) ON GLIAL-CELL DEVELOPMENT IN RAT OPTIC-NERVE

被引:37
作者
PHILLIPS, DE [1 ]
KRUEGER, SK [1 ]
机构
[1] MONTANA STATE UNIV, WAMI, MED EDUC PROGRAM, BOZEMAN, MT 59717 USA
关键词
OLIGODENDROCYTE; ALCOHOL; ETHANOL; OPTIC NERVE; FETAL ALCOHOL SYNDROME; RAT; DEVELOPMENT; NEUROGLIA;
D O I
10.1016/0736-5748(92)90059-9
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
This study evaluated the effects of a combined gestational and 10 day postnatal alcohol exposure (human three trimester equivalency) on the development of glial cells in the rat optic nerve. Pregnant rats were exposed to alcohol via a liquid diet, then their pups were artificially reared and further exposed to alcohol for 10 postnatal days via a gastrostomy fed liquid diet. Control animals, born of pair fed dams, were artificially reared on pair fed isocaloric diets. Optic nerve tissues were prepared for light and electron microscopic studies from animals on gestational days (G) 15 and 20 and postnatal days (P) 5, 10, 15, 20 and 90. There were fewer glial cells per cross-section on day 15 and the cross-sectional areas of optic nerves were smaller on days G20, P15 and P90 in the ethanol exposed animals. There was an alcohol-induced delay in the appearance of immature cells within the oligodendroglia lineage and a decrease in the number of oligodendroglia present at 15 and 20 days, indicating a delay in the maturation of oligodendroglial cells. These effects were compensated for by 90 days. Maturation of the astrocytic cell lineage was generally unaffected by the alcohol although there was evidence of increased numbers of cells in the lineage. There was no consistent indication of alcohol-induced degeneration of glial cells or their organelles. Thus, alcohol exposure for all of gestation and 10 postnatal days in the rat causes a delay in oligodendrocyte maturation but appears to have no long-term effects on the glial cell population of the optic nerve. Such a delay, by contributing to delays in myelin development, could help to explain some of the neurological dysfunctions associated with developmental alcohol exposures.
引用
收藏
页码:197 / 206
页数:10
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