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Chunk #14 — Results — Decreased neurogenesis after binge alcohol exposure

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Alcohol inhibition of neurogenesis: a mechanism of hippocampal neurodegeneration in an adolescent alcohol abuse model.
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Well-accepted markers of adult neurogenesis were examined through immunohistochemistry on tissue from various time points during and after binge alcohol administration. To determine whether alcohol affected neurogenesis in an adolescent model of AUD, DCX expression was examined at various time points in the dorsal dentate gyrus. DCX is expressed transiently by migrating neuroblasts from a few to several days after a cell divides (Brown et al., 2003; Gleeson et al., 1999). As shown in Figure 2, DCX-positive cells were observed throughout the superior and inferior blades of the dentate gyrus of the hippocampus in both the control and alcohol exposed subjects. Because DCX immunohistochemistry was processed in batches by timepoint, each time point was analyzed independently for differences in pixels/μm2 but presented together as percent of control in Figure 2a. Assessment of DCX+IR showed, a 35 ± 3.9% decrease (p<0.05) after four consecutive days (4D) of alcohol exposure (Con= 0.159143 ± .021 pixels/μm2, n=6; EtOH= 0.107303 ± .006 pixels/μm2, n=6) and a 27.9 ± 9.1% decrease (p<0.05) for 4D+2 group (Con= 0.134994 ± .008 pixels/μm2, n=7; 4D+2= 0.097371 ± 0.012