several protein kinases, including, CaMKII, PKC and PKA, which alter AMPA-type glutamate receptor phosphorylation, and insertion of GluR1-containing AMPA receptors into synapses [48]. Learning and memory functions dependent on the neocortex are impaired in subjects with moderate to severe AUDs, and rodent studies have demonstrated aberrant metaplasticity of NMDAR dependent form of synaptic plasticity in the neocortex in vitro [49]. In addition, studies in human subjects have demonstrated impaired LTP-like neuroplasticity in the neocortex in vivo in intoxicated individuals [50]. Together these findings suggest the hypothesis that EtOH-induced alterations in both forms of synaptic plasticity in the neocortex (discussed in later sections) could contribute to the behavioral deficits seen in individuals with AUDs.
