of GR expression correlated with the development of depressive-like phenotypes, including anhedonia and helplessness (105), and reduced hippocampal neurogenesis (104). Further, there are several lines of evidence that suggest that downregulation of BDNF–TrKB–CREB signaling pathway may serve as a common link between the development of alcohol-induced depression-like symptoms and reduced hippocampal neurogenesis (104, 105, 107, 108). Finally, since enhancing the BDNF–CREB activity through pharmacological treatments with various classes of antidepressant drugs or environmental enrichment abolished the alcohol-induced anhedonia and depressive behaviors seen during protracted abstinence (104, 107, 108), supporting the hypothesis that BDNF–CREB signaling pathway may be a potential therapeutic target for interventions in alcoholism–depression coincidence.
