Ethanol alters learning and memory (Oslin and Cary, 2003; White, 2003), and this may involve effects on synaptic plasticity, including long-term depression (LTD) and long-term potentiation (LTP) (reviewed in Zorumski et al., 2014). Most of the data on ethanol effects on synaptic plasticity come from studies in the hippocampus. Acute ethanol inhibits LTP in hippocampal slices (Blitzer et al., 1990; Morrisett and Swartzwelder, 1993), but these results are not consistent (Fujii et al., 2008; Swartzwelder et al., 1995). This variability may be due to many factors, including age, subregion, and stimulus strength. Acute ethanol blocks LTP in apical dendrites but only reduces LTP in basal dendrites (Ramachandran et al., 2015). These effects may be due to NMDAR inhibition (Chandler et al., 1998; Izumi et al., 2005), but recent work posits a role for neurosteroids (Izumi et al., 2015; Tokuda et al., 2013). In contrast to LTP, hippocampal LTD is enhanced by acute ethanol in the CA1 region (Hendricson et al., 2002), and this effect involves NMDARs and mGluR type 5 (mGluR5) (Izumi and Zorumski, 2012; Overstreet et al., 1997) (Figure 2T).
