Effect of Voluntary Exercise on c-Fos expression in Adult-born New Neurons in Hippocampal Dentate Gyrus of Rats Exposed to Alcohol Neonatally
Date
2013-05
Authors
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Publisher
University of Delaware
Abstract
Our lab uses a rodent model of Fetal Alcohol Spectrum Disorder to observe
how neonatal alcohol exposure effects neuroplasticity during development, as well as behavioral therapies that might ameliorate such damage. Using a rodent model of third trimester binge drinking on postnatal days (PD) 4-9, our lab observed decreased the number of adult-born, mature neurons surviving in the adult hippocampal dentate gyrus (DG) (Klintsova et al., 2007). Rats with access to voluntary exercise show enhanced cell proliferation at PD42 in dentate gyrus (DG) in control and alcohol exposed (AE) animals. However at PD72 AE animals show no long-term benefit of wheel running in looking at the newly generated cells (Helfer et al., 2009). To investigate mechanisms underlying decreased cell survival in AE animals after wheel running, we use an immediate early gene, c-Fos, to capture subtle changes in activation patterns within the hippocampal regions CA1, CA3, and DG at PD42. CFos induction, which past studies have shown to be previously impaired following AE, increases with bouts of stimulation such as wheel running (Clark et al., 2011). C-Fos identifies active neurons, which may have a functional role in the hippocampal circuit. On PD4, rats are assigned to either the suckle control (SC), sham intubated (SI) or alcohol exposure (AE) treatment group. On PD4-9 AE rats are exposed to a milk/ethanol solution (5.25 g/kg ethanol per day) via intragastric intubation in a bingelike manner. During PD30-42, rats are placed in either standard social housing (SH) or voluntary wheel running (WR; 24 hr access). Tissue was stained using a c-Fos antibody and analyzed on a light microscope using unbiased stereological techniques.