The PFC is involved in the cognitive symptoms of AUD. Although studies have investigated the acute effects of ethanol on PFC NMDARs (Weitlauf and Woodward, 2008), few have investigated the effect on synaptic plasticity in this area. Chronic ethanol exposure induces an increase in the NMDA/AMPA current ratio in the PFC and enhances expression of NMDAR-mediated spike-timing-dependent LTP, a neuroadaptation likely associated with reduced behavioral flexibility (Kroener et al., 2012; Nimitvilai et al., 2016a) Figures 3K–3L). It will be interesting to determine how these plasticity changes contribute to ethanol-induced cognitive impairment.
