Central and peripheral neurochemical alterations and immune effects of prenatal ethanol exposure in rats

Abstract

In contrast to the well known effects of prenatal ethanol exposure on the central nervous system, data about its peripheral effects are scarce. Here, Sprague Dawley rats were fed a liquid diet (gestational days 0-20) containing 36% ethanol-derived calories (EDCs, group H) or were pair-fed with 18% EDCs (group L) or 0% EDCs (group C). On postnatal day 20, one male and one female from each of 10 litters per group were killed. Norepinephrine (NE) was analyzed in the frontal cortex, spleen and thymus, and dopamine, 5-hydroxytryptamine (serotonin, 5-HT) and their metabolites 3,4-dihydroxyphenylacetic acid, homevanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) were analyzed in the striatum by high-performance liquid chromatography with electrochemical detection. Lymphocyte subpopulations in the spleen and thymus were also assessed in half of these litters. Significant decreases in splenic NE concentration were seen in both sexes of group H (males 27%, females 28%). Decreases in striatal 5-HT and 5-HIAA of group H subjects appeared to be sex specific (only females were significantly affected: 23% decrease in 5-HT, 37% decrease in 5-HIAA). Pronounced, dose-dependent reductions in T cell percentages were observed in both the thymus and spleen. Splenic CD8+ and CD4+ cell percentages were positively correlated with the splenic NE concentrations. It is concluded that the decreases seen in splenic T cell percentages subsequent to prenatal ethanol exposure may be caused, at least partially, by impaired noradrenergic control of this organ.

Prenatal ethanol exposure in rats alters serotonergic-mediated behavioral and physiological function

“…Zafar et al (2000) found that 21-day-old E females had a transient decrease in 5-HT transporter binding sites in the hypothalamus compared to control females, although 21-day-old male offspring were not affected. Clausing et al (1996) found a decrease in striatal 5-HT and 5-HIAA in 20-day-old E females, but not in E males. A third study found that females exposed to ethanol in the early postnatal period (third trimester equivalent) showed increased basal levels of septal 5-HT and 5-HIAA in adulthood (Kelly 1996).…”

Effects of Prenatal Exposure to Alcohol on the Release of Adenocorticotropic Hormone, Corticosterone, and Proinflammatory Cytokines

“…The fact that no significant differences were observed in cytokine response to various immune challenges in C and E animals has important implications. It suggests that changes in the release of these cytokines probably does not underlie the altered immune function that has been observed in animals that have been exposed to alcohol prenatally (Gottesfeld et al, 1990;Gottesfeld and Ullrich, 1995;Chiappelli and Taylor, 1995;Giberson and Weinberg, 1995;Clausing et al, 1996;Jerrells and Weinberg, 1998).…”

Age and Gender Differences in Response to Neonatal Ethanol Withdrawal and Polyamine Challenge in Organotypic Hippocampal Cultures

“…Data primarily from these animal models have shown that perinatal ETOH exposure can affect virtually every neurotransmitter and neuromodulator that has been studied including the monoamines dopamine, norepinephrine, and serotonin (e.g. Boggan et al, 1996;Clausing et al, 1996;Maier et al, 1996;Shen et al, 1999;Sobrian et al, 2005;Tran and Kelly, 1999;), adenosine (Othman et al, 2002), the neurosteroids, opioids (Angelogianni and Gianoulakis, 1989) and the amino acid transmitters GABA and glutamate (GLU) (e.g. Diaz-Granados et al, 1997;Hsiao et al, 1998;Spuhler-Phillips et al, 1997).…”