apoptotic. FJB labeling and pyknotic nuclei are observed throughout the apoptosis-necrosis spectrum of cell death and cannot be used to differentiate the mechanism of cell death. However, TUNEL is a well-accepted marker of apoptosis (Gavrieli et al., 1992) and the lack of TUNEL labeling is consistent with necrosis as the mechanism of cell death in binge alcohol exposure (Obernier et al., 2002). Intriguingly, this level of cell death, i.e. a few cells per section, would not be expected to contribute significantly to volume loss. However, a sustained 50% decrease in neurogenesis could, especially if neurogenesis were decreased for several days. Alcohol induced inhibition of neurogenesis results in an estimated cell loss that is identical to that reported after chronic alcohol exposure (Nixon and Crews, 2002; Walker et al., 1980). Thus, these data when considered altogether strongly support that inhibition of neurogenesis - both reduced proliferation and reduced cell survival - may be a mechanism that contributes to volume loss in adolescents with an AUD.
