Changes in subcellular distribution of receptors may also contribute to altered NMDAR function following chronic EtOH exposure. In cultured hippocampal neurons, exposure to EtOH leads to increased NMDAR expression in dendritic spines, the location of glutamatergic synapses (Carpenter-Hyland et al. 2004). This increased trafficking to spines is accompanied by an increase in the contribution of NMDARs to glutamatergic transmission, but does not appear to involve increased NMDAR protein expression. The synaptic NMDARs observed following chronic EtOH exposure appear to contain the NR2B subunit. Increases in the contribution of NMDARs to glutamatergic synaptic transmission have also been observed following subacute (10 s of seconds or minutes) EtOH exposure, and NR2Bcontaining receptors also appear to contribute to these increases (Wang et al. 2007; Yaka et al. 2003). Tyrosine phosphorylation by a Fyn-like kinase has been implicated in these rapid increases in the function of NR2B-containing receptors (Wang et al. 2007), but it is yet to be determined whether this mechanism plays a role in chronic EtOH effects on the receptor.
