Ethanol exposure affects DNA methylation in glia and increases tissue plasminogen activator (tPA) expression, which is involved in the inhibition of neuritogenesis and regulates neuronal plasticity (Zhang, Kusumo, Sakharkar, Pandey, & Guizzetti, 2014). Additionally, amygdaloid tPA has been implicated in regulating stress responses during acute cocaine withdrawal (Zhou, Maiya, Norris, Kreek, & Strickland, 2010). These examples illustrate the importance that glial and neuronal compartments be considered as not discrete entities, but rather as highly inter-connected structures which collaboratively influence neuronal plasticity (Todd, Serrano, Lacaille, & Robitaille, 2006). Dissecting out the epigenetic pathways in glia and neurons involved in chronic drug-induced neuroinflammation and synaptic plasticity will provide increased treatment opportunities to address the neuroinflammatory changes following chronic ethanol exposure (Kovacs, 2012).
