Developmental Brain Research, 38 (1988) 161-166 161 Elsevier BRD 50669 Research Reports Effects of short-term prenatal alcohol exposure on neuronal membrane order in rats Charles V. Vorhees 1, Scott Rauch 2, and Robert Hitzemann 1 llnstitute for Developmental Research, Children's Hospital Research Foundation, and Department of Pediatrics, University of Cincinnati, Cincinnati, 0H45229 (U.S.A.) and 2Department of Psychiatry, University of Cincinnati, Cincinnati, 0H45267 (U.S.A.) (Accepted 7 July 1987) Key words: Prenatal alcohol; Brain neuronal membrane order; Brain membrane fluidity and development; Ethanol and brain neuronal membrane Long-Evans rat dams were treated with ethanol (4 g/kg, twice daily) by gavage on gestational days 10-14. This dosage schedule has been shown to produce significant behavioral and ponderal teratogenicity. Pair-fed dams were gavaged with isocaloric amounts of su- crose. All offspring were reared by untreated, surrogate dams. Pups were sacrificed on days 3 and 28, and whole brain neuronal plas- ma membranes were prepared for analysis by a fluorescence polarization technique using 1,6-diphenyl-l,3,5-hexatriene as the mem- brane probe. On day 3, steady-state anisotropy was significantly decreased in the ethanol-treated pups. Arrhenius plots revealed that this difference was associated with a change on both membrane entropy and enthalpy. By day 28, the differences between groups dis- appeared. These data would be consistent with the view that the brief gestational ethanol exposure delays neuronal maturation. INTRODUCTION It is now clear that alcohol is both a behavior- al 1'2'29'37'40 and structural teratogen H,25,32. The be- havioral effects can be seen at alcohol exposure lev- els below those required for overt structural malfor- mations. Some of the most common behavioral ef- fects of fetal alcohol exposure have included in- creased activity or reduced locomotor habituation using the open-field 6,7,9A°,17,18,30 and holeboard34; re- duced avoidance performance using conditioned taste aversion 3-s, one and two-way active avoid- ance 8'38, and passive avoidance3,16,35; increased reac- tivity using auditory startle4; reduced appetitive dis- criminationS; increased perseverative behavior using T-maze learning or spontaneous alternation36; and delayed reflex and physical development using tests of n¢gative geotaxis, surface righting, and eye open- ing2~,28, 38. Recently, we have examined the behavioral and ponderal teratogenicity associated with a discrete al- cohol exposure during days 10-14 of gestation 41. Ethanol-exposed offspring exhibited delayed olfac- tory orientation to home cage scent and delayed low- er incisor eruption compared to pair-fed or ad lib fed controls. After weaning, the ethanol offspring exhi- bited increased open-field activity, particularly of centrally located sections, and facilitated swimming performance in a water maze. Ethanol-exposure sig- nificantly decreased weight gain and increased post- natal, but not prenatal, mortality in the progeny. The female ethanol offspring also showed delayed vaginal patency development. The biochemical mechanisms underlying the be- havioral abnormalities associated with short and/or long-term prenatal ethanol-exposure are unknown. Current theories suggest that ethanol acts by disrupt- ing (perturbing) the neuronal membrane lipid ma- Correspondence: R. Hitzemann. Current address: Department of Psychiatry and Behavioral Science, State University of New York at Stony Brook, Health Sciences Center, Stony Brook, NY 11794-8101, U.S.A. 0165-3806/88/$03.50© 1988 Elsevier Science Publishers B.V. (Biomedical Division)