The voltage-gated sodium channel is another putative quantitative trait gene for alcohol drinking behavior (Davies et al., 2003; Mulligan et al., 2006). In the prefrontal cortex of human alcoholics, three high confidence transcripts for the voltage-gated sodium channel (SCN4B, SYT13, and TBC1D9) correlated with lifetime alcohol consumption (Farris and Mayfield, 2014). In neurons, SCN4B can override the effects of other beta subunits (Yu et al., 2003), modify sodium channel firing rates (Grieco et al., 2005), and structurally alter neuronal projections (Oyama et al., 2006). There are three coding isoforms of SCN4B in humans, but only the shortest coding variant (NM_001142349) was significantly correlated with alcohol consumption (Farris and Mayfield, 2014). WGCNA identified this variant as a phenotypic focal point within the network that was distinct from the other two coding isoforms of SCN4B (Farris et al 2014). NM_001142349 was positively co-expressed with another splicing variant, SCN8A, a sodium channel alpha subunit expressed within neuronal synapses (Farris and Mayfield, 2014; Schaller and Caldwell, 2000). Although the positive co-expression of SCN4B and SCN8A splice variants may signify their functional importance, this is
