Several recent studies have shown that alternative splicing is correlated to chronic alcohol consumption. Chronic self-administration of alcohol in cynomolgus macaques (Macaca fascicularis) is associated with alternative splicing of AMPA subunits in the prefrontal cortex (Acosta et al. 2012). Broader transcriptomic analysis demonstrated overrepresentation of genes associated with splicing across brain regions in chronic ethanol self-administrating rhesus macaques (Macaca mulatta) (Iancu et al. 2018). Similar alcohol-induced effects on splicing extend to humans (Farris and Mayfield 2014). Postmortem analysis of the brains of patients with AUD showed novel splicing in GABAB1 that decreased expression of the GABA binding site (Lee et al. 2014). Similarly, alcohol-induced splicing events also occurred in the developing human cortex in utero, potentially resulting in devastating neurodevelopmental consequences (Kawasawa et al. 2017).
