Using our limited-access, moderate prenatal alcohol exposure (PAE) paradigm (Brady et al., 2012), we found that alcohol significantly (p < .05) decreased expression of several neurogenic factors involved in development and function of the central nervous system, particularly mechanisms associated with cell growth and death (Table 1). These include Adora2a, Cxcl1, Dlg4 (PSD-95), Hes1, Nptx1, and Vegfa (Fig. 3). Several of these genes have been studied in the context of alcohol exposure; for example, Adora2a, which encodes the A2A receptor and is highly expressed in the adult striatum, has been implicated in alcohol use disorders and other addictive behaviors (Hack & Christie, 2003; Nam, Bruner, & Choi, 2013; Nam, Hinton, et al., 2013). Transient expression of A2A during development of the brain aids in neuritogenesis and proliferation (Sun et al., 2010; Weaver, 1993); however, the role of A2A in development after PAE has not been studied extensively. Additionally, A2A activation leads to upregulation of VEGF expression, suggesting that the decreased mRNA levels of both of these genes after PAE may be connected in the proliferating NPC culture conditions (Escudero et
