(Okubo-Suzuki et al., 2008), supports the idea that some form of ethanol-induced synaptic plasticity may have occurred within the ACB-shell of P rats. In contrast to the up-regulation of Ngef and Synpo, the protein expression level of the Ras GTPase-activating protein SynGap (Syngap1), which appears to have a role in LTP and is associated with NMDA receptors (Komiyama et al., 2002), was significantly reduced in the ACB-shell. However, in cultured neurons, over-expression of Syngap reduced AMPA receptor function and insertion of AMPA receptors into the plasma membrane (Rumbaugh et al., 2006). Therefore, in the present situation, it is possible that reduced levels of Syngap could results in enhanced AMPA receptor function. The findings that ethanol-induced synaptic plasticity may have occurred in the ACB-shell of both P and NP rats, but that different proteins are involved, suggest that different synaptic events have occurred, possibly involving alterations in different synaptic connections in the two rat lines.
