Fetal ethanol exposure diminishes hippocampal beta-adrenergic receptor density while sparing muscarinic receptors during development

Because of ostensible effects of fetal exposure to ethanol on cardiac and memory functions, beta-adrenergic and muscarinic receptor binding were surveyed in hippocampus and heart in 8- and 17-day-old rat pups. Pregnant, multiparous rats were intubated with either 6 g/kg ethanol or isocaloric dextrose twice daily from gestational days 10-16. At birth, offspring were fostered to untreated mothers. Pups exposed to ethanol had diminished birth weights, although there was no difference in the amount of weight gain by ethanol and control dams during gestation, nor in litter size. Ethanol pups remained smaller than control pups, but this difference was significant only until 8 days of age. At 17 days of age, ethanol pups had fewer hippocampal beta-adrenergic receptors than age-matched controls; muscarinic receptors and CA1 cell densities were not disparate. Parallel studies suggested that approximately 50% of the hippocampal beta-adrenergic receptors in 8-day-olds were of the beta 1 and beta 2 subtypes, while by 17 days of age approximately 70% of the receptors were beta 1. There was an ontogenetic increment in both beta-adrenergic and muscarinic binding from 8 to 17 days of age in hippocampus. No differences between age or drug groups were found in the binding measures in heart tissue. The present findings indicate that fetal ethanol treatment affects developmental measures and beta-adrenergic receptors in the hippocampus in a quasi-selective manner, but not hippocampal CA1-cell density.