Prenatal Alcohol Exposure in Rats Diminish Postnatal Cxcl16 Chemokine Ligand Brain Expression

Maternal ethanol consumption during pregnancy is one of the main causes of Neurodevelopmental disorders (NDD). Prenatal alcohol exposure (PAE) produces several adverse manifestations. Even low or moderate intake has been associated with long lasting behavioral and cognitive impairment in offspring. In this study we examined the gene expression profile in the rat nucleus accumbens using microarrays, comparing animals prenatally exposed to ethanol and controls. The microarray gene expression showed an overall downward regulatory effect of PAE. Gene cluster analysis reveals that the main affected gene groups are related to transcription regulation, transcription factors and homeobox genes. We focus on the expression of the C-X-C motif chemokine ligand 16 (Cxcl16) which was differentially expressed. There is a significant reduction in the expression of this chemokine throughout the brain under PAE conditions, evidenced here by qPCR and immunohistochemistry. Chemokines are involved in neuroprotection and implicated in alcohol-induced brain damaged and neuroinflammation in the developing CNS, therefore, the significance of the overall decrease in Cxcl16 expression in the brain as a consequence of PAE, may reflect a reduced ability to neuroprotection against subsequent conditions, such as excitotoxic damage, inflammatory processes or even hypoxic-ischemic insult. Transcriptional profiling of rat nucleus accumbens comparing rats prenatally exposed to ethanol (EtOH) with control isocaloric solution (ISO). Microarray analysis was performed on pools of seven rats for each group (i.e. seven ISO, seven EtOH) to compensate for inter-organism variability in an heterologous hybridization.