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. Author manuscript; available in PMC: 2015 Oct 3.
Published in final edited form as: Prog Neuropsychopharmacol Biol Psychiatry. 2014 May 17;0:103–113. doi: 10.1016/j.pnpbp.2014.05.003

Figure 1.

Figure 1

Schematic representation of adult neurogenesis and known ways in which alcohol affects this process. Adult hippocampal neurogenesis consists of multiple stages that cells progress or mature through: stem-like radial glia act as the neural stem cell (NSC) and proliferate into neural progenitor cells (NPCs). Type 1 radial-glia like neural stem cells divide asymmetrically and produce a progenitor (Type 2a) that can also divide and produce daughter progenitors (circular arrows indicate that the cell is capable of replicating). The NPC term is used throughout when it is not clear which cell type, the NSC or one of the progenitors, has been examined or if the distinction was not made. These subpopulations of progenitors have varying capacities for self-renewal and differentiation as NPCs may differentiate into a neuronal or glial phenotype (Bonaguidi et al., 2011; 2012; Dranovsky et al., 2011; Encinas et al., 2011). The maturation of these cells progress through Type 3 and immature neuroblast (I) as they migrate and integrate into the granule cell layer (GCL) where they finally become mature granule cells (M; green cells = granule cells; pink cells = SGZ; Gage, 2000; Zhao et al., 2008). Alcohol impacts these processes at multiple stages:
  1. Alcohol dependence may kill progenitor cells with long duration, chronic exposure (Richardson et al., 2009; Taffe et al., 2010).
  2. Alcohol intoxication reduces NPC proliferation whereas reactive increases in neurogenesis occur at one week in abstinence (Nixon and Crews, 2002; 2004). Alcohol also alters the cell cycle of NPCs (McClain et al., 2011a).
  3. Multiple ways in which alcohol may directly affect the neurogenic niche, notably alcohol produces reactive astrocytes and reactive microglia (Kelso et al., 2011; Marshall et al., 2013; McClain et al., 2011b).
  4. High peak blood ethanol concentrations are likely required to impact survival of new born cells (Herrera et al., 2003; Nixon and Crews, 2002).
  5. Chronic alcohol exposure blunted dendritic arborization in newborn cells (He et al., 2005), an effect that would have functional implications for new cells incorporation into hippocampal circuitry.
  6. Binge alcohol exposure kills entorhinal cortex cells that project to the hippocampal dentate gyrus (Collins et al., 1996; Kelso et al., 2011).