Chunk #29 — Potential Biological Mechanism of Hippocampal Sensitivity to AUDs: Impact of Altered GluN and GABAR Signaling in the Hippocampus on Adult Neurogenesis — Regulation of Neurogenesis by Alcohol
In addition to a general understanding of neurogenesis, we are beginning to understand how alcohol exposure impacts hippocampal neurogenesis and what this may imply for cognitive performance and capacity (see Figures 1A–C for a summary). For example, while cellular proliferation and neurogenesis are reduced during excessive alcohol-induced dependence (167–169), early withdrawal from excessive alcohol is documented to result in an increase in cellular proliferation in the DG (169–171). The survival capacity of progenitors born during this period of increased proliferation and their functional importance is still unclear; however, reports using alcohol gavage [blood alcohol levels (BALs) reaching >400 mg%] demonstrate increased survival of newly born neurons subsequent to the proliferative burst (170, 173, 174). In contrast, animals made dependent to alcohol via ethanol vapor exposure (BALs maintained between 150–250 mg%) demonstrate a marked reduction in the number of surviving young neurons in the DG (169, 171). This difference could be attributed to differences in BALs and negative affect symptoms resulting from the exposure paradigm (gavage vs. CIE). Unfortunately, there is no conclusive evidence linking aberrant neurogenesis subsequent to alcohol dependence
