Our research suggests that kainate receptors in the BLA, like NMDA and AMPA receptors, actively participate in the overall increase in glutamatergic function in response to chronic ethanol exposure. Specifically, chronic intermittent ethanol increases KA-R-mediated synaptic responses in the BLA. In fact, this ethanol-dependent increase in KA-R function during CIE might contribute to glutamatergic synaptic plasticity during either CIE or WD. This is consistent with previous findings that repeated ethanol withdrawal causes synaptic strengthening in the amygdala and occludes BLA long-term plasticity (Stephens et al., 2005). Saturation of LTP has been shown to impair fear learning (Moser et al., 1998) but leads to generalized increases in anxiety-like behavior. We have recently shown that BLA-dependent processes contribute to this withdrawal-associated anxiety (Lack et al., 2007). Therefore, occlusion of ATPA-induced synaptic plasticity by CIE and WD may suggest that KA-R mediated plasticity could contribute to withdrawal-related anxiety.
