(Figure 6) were combined with phenotype percentages (Figure 5), a nearly 50% reduction in neurogenesis was estimated at four weeks after the last dose of alcohol. Although the loss of BrdU+ signal at D4+28 days could in theory be due to signal dilution, other groups have shown that loss of BrdU is due to cell death (Cameron and McKay, 2001; Dayer et al., 2003). This interpretation is also consistent with prior work in adult rats where chronic alcohol ingestion reduces new cell survival specifically (He et al., 2005; Herrera et al., 2003). Furthermore, alcohol significantly increased three markers of cell death, FJB, Pyknosis, and TUNEL staining, which supports inhibited cell survival as the most plausible interpretation of decreased BrdU-labeled cells. In summary, this dual impact on hippocampal integrity - alcohol induced inhibition of cell proliferation and newborn cell survival - could contribute to hippocampal volume loss observed in adolescents diagnosed with an AUD (De Bellis et al., 2000).
