γ-Linolenic Acid Fails to Prevent the Effects of Prenatal Ethanol Exposure on Brain and Behavioral Development in B6D2F2Mice

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Abstract
The purpose of this study was to obtain a quantitative assessment of the behavioral retardation caused by prenatal ethanol exposure in mice and to test the hypothesis that .gamma.-linolenic acid (GLA) supplementation would prevent such effects. Pregnant B6D2F1 mice were fed liquids diets containing 25% ethanol-derived calories from days 7-17 of gestation. The experimental groups were given GLA via s.c. injection; the control was administered vehicle only. All groups were pair fed to this ethanol control, including a 2nd control group which received sucrose substituted isocalorically for ethanol. Additional control groups included 1 fed lab chow ad libitum and 2 further ethanol groups, 1 treated with coconut oil, the other with arachidonic acid (AA). Behavioral development of the pups was measured on day 32 postconception and open field behavior was measured on day 50. Body and brain wt were also measured. Reproductive outcome, as measured by animals which produced live pups, was worse in the GLA- and AA-treated groups. Ethanol produced significant behavioral retardation of the order of 1.7 days. Body and brain wt were lower in ethanol-treated pups. Covariance analysis indicated that the effect on brain wt was independent of the effect on body wt. Open field scores suggested that ethanol-treated males were more active than sucrose controls. The data did not support the hypothesis that GLA would prevent the deleterious effects of prenatal ethanol exposure; in no instance was a GLA-treated group different from the ethanol control.