Previous research in our lab showed that BLA kainate receptors and kainate receptor-mediated synaptic plasticity are inhibited by acute ethanol (Lack et al., 2008). This suggests that the up-regulation of KAR-mediated synaptic responses in chronic ethanol-exposed neurons arises from this acute sensitivity. Although the mechanism responsible for this up-regulation is not currently known, it was apparently transient since KAR-mediated synaptic responses returned to baseline following twenty four hours of withdrawal. This rapid return would suggest that changes in gene or protein expression levels are less-likely potential mechanisms. Unfortunately, there is little guidance in the literature with respect to the effects of chronic ethanol/withdrawal on kainate receptors. Previous findings have been inconsistent and shown either no effect of chronic ethanol on kainate receptor subunit protein levels (Chandler et al., 1999; Ferreira et al., 2001) or up-regulation during withdrawal (Carta et al., 2002). These contrasting findings likely reflect the diversity of experimental approaches (e.g. native versus in vitro systems) and ethanol exposures.
