The ethanol-induced reductions in hippocampal neurogenesis can be attributed to two general mechanisms: an effect on cell proliferation or on cell survival. These changes in the hippocampal structure could be part of the anatomical basis for the cognitive deficits described in alcoholism. The hippocampus is a target site for the teratogenic effects of ethanol (West and Pierce 1986). Morphological changes in this brain region may play a critical role in the manifestation of mental deficiency and behavioral abnormalities in individuals with fetal alcohol syndrome or alcohol-related neurodevelopmental disorder (Institute of Medicine 1996). There is evidence that certain hippocampal neuronal cell types are particularly sensitive to ethanol teratogenicity. Chronic exposure of the developing HP to ethanol can result in selective damage, such as a decrease in the number of CA1 pyramidal cells in the adult pig (Abdollah et al 1993; Gibson et al 2000) and rat (Bonthius and West 1990; Miller 1995). One study of human alcoholics aged 45 years and under, reported an early neuronal loss of the dentate gyrus and the ammonic fields CA1 through CA4 (Bengochea and Gonzalo 1990), and another study found glial cell loss (especially astrocytes and oligodendrocytes) in the hippocampus of alcoholics (Korbo 1999).
