Exposure to alcohol in utero has been associated with long-term immune deficits. In addition, adult mice exposed to alcohol prenatally display altered noradrenergic synaptic transmission selectively in lymphoid organs. This is consistent with the hypothesis that sympathetic neurons play an important role in immunomodulation. The development and maintenance of sympathetic neurons are critically dependent on nerve growth factor (NGF). Furthermore, NGF has been shown to modulate immune responses and NGF receptor expression has been localized to lymphoid organs. The present work examined the effects of prenatal alcohol exposure on the development and maturation of pre- and postsynaptic sympathetic components, including norepinephrine and beta-adrenoceptors, respectively, as well as the early expression of NGF receptors in lymphoid and other organs of the C57BL/6 mouse. Infant mice that were exposed to alcohol in utero displayed reduced levels of norepinephrine and beta-adrenoceptor density, as well as increased NGF receptor expression in the thymus and spleen, but not the heart. These selective changes may account, in part, for the persistent immune incompetence characteristic of fetal alcohol syndrome.