Prenatal ethanol exposure alters immune capacity and noradrenergic synaptic transmission in lymphoid organs of the adult mouse.

Clinical and experimental evidence indicates that exposure to alcohol in utero is associated with altered immune capacity. The mechanisms underlying such abnormalities are not clear. However, the suggestion that reciprocal interactions between the immune and the nervous systems are necessary for a competent immune response may be relevant. This work examined the consequences of prenatal ethanol exposure on cellular immune responses and noradrenergic synaptic transmission in lymphoid organs of the adult C57B1/6 mouse. Pregnant mice were fed a liquid diet containing 25% of the calories as ethanol (4.8% w/v) or pair-fed an isocaloric equivalent of this diet throughout gestation, followed by foster-nursing the neonates on normal dams. As young adults, mice exposed to ethanol prenatally displayed immunologic and selective neurochemical changes: (1) depressed ability to produce cellular immune responses, including contact hypersensitivity and a local graft-vs-host response, and (2) altered noradrenergic synaptic transmission, including enhanced norepinephrine turnover, and a reduction in norepinephrine levels and beta-adrenoceptor density in the thymus and spleen, but not the heart. However, both the integrity and compartmentation of noradrenergic nerve fibres in the spleen were intact. It is suggested that altered noradrenergic synaptic transmission selectively in lymphoid organs may contribute to the impaired immune capacity associated with fetal alcohol exposure.