Effect of Neonatal Alcohol Exposure on C-Fos Expression in Hippocampal Ca3 Followingexploration of Novel Context in Adolescence

Modlin, Samuel
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University of Delaware
In humans, developmental alcohol exposure (AE) results in a myriad of deficits across several domains of human functioning that persist across the lifespan of the afflicted individual. This issue warrants thorough study, as prenatal AE affects millions of children across the globe every year. The present study uses a rodent model of fetal alcohol spectrum disorders (FASD) to examine the effect of third-trimester equivalent (post-natal day 4-9) alcohol exposure on the density of cells c-Fos as an indirect measure of neuronal activity, in adolescent rats following exploration in a novel context. Rats were exposed to one of three dosing conditions: Two AE groups, exposed in a single binge dose (4.0 g/kg/day or 5.25 g/kg/day), and a sham intubated (SI) group to control for the stress of the alcohol administration procedure. Novel context exposure has been shown to generate c-Fos expression in the hippocampus, at levels correlated with acquisition of a fear-response in a conditioning task in that context (Radulovic, Kammermeier, & Spiess, 1998). Prior experiments have shown hippocampal c-Fos expression and contextual fear conditioning is reduced in animals exposed to alcohol neonatally (Murawski, Klintsova & Stanton, 2012). In CA1, following exploration of a novel context, both total pyramidal cell count and the number of cells expressing c-Fos was decreased in AE animals relative to controls (Murawski et al., 2012). The present study assessed the effect of neonatal AE the density of c-Fos+ cells/mm2 of CA3 using optical densitometry, examining the same tissue assessed by Murawski and colleagues (2012). The present study found a trending increase in c-Fos+ density in dorsal CA3 in the higher AE group (5.25g/kg/day) compared to SI controls. Differences between groups in total and ventral CA3 c-Fos+ were insignificant. This data may provide useful insight into the pathology of hippocampal circuitry as a result of neonatal AE.