The effects of prenatal ethanol exposure on N-methyl-D-aspartate (NMDA)-mediated calcium entry into neonatal dissociated neurons from hippocampus, forebrain, and cerebellum were investigated. Dissociated cells were isolated from less than 1-day-old pups of prenatally exposed, pair-fed control and ad libitum control groups and loaded with fura-2. Prenatal ethanol exposure significantly reduced the NMDA-stimulated increase in intracellular calcium in all three brain regions compared to the two control groups. These findings are very similar to those previously observed in neonatal dissociated whole brain neurons using the same ethanol exposure protocol. Studies were also conducted using forebrain to determine if prenatal ethanol exposure alters NMDAR1 subunit protein expression in this major brain area; however, the results indicated no significant differences between ethanol-exposed and control groups.
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Spuhler‐Phillips et al. (1997) studied this question.
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