In summary, the current work provides the first evidence of facilitation of kainate receptor synaptic function by chronic ethanol. This facilitation is contrasted with the occlusion of ATPA-mediated synaptic plasticity during both CIE and withdrawal. The overall increase in neurophysiologic responses during CIE and WD indicates that this occlusion results from a CIE/WD-dependent recruitment of the cellular mechanisms that govern the expression of synaptic plasticity within the BLA. This interpretation is supported by previous findings showing diminished activity-dependent synaptic plasticity in the BLA following alcohol exposure/withdrawal (Stephens et al., 2005). With respect to downstream efferent areas like the central amygdala and the bed nucleus of the stria terminalis, the precise ramifications of this alcohol-dependent recruitment are not yet know. However, we hypothesize that the increased responsiveness of BLA neurons (evidenced by the fEPSP data) might be manifested as increases in glutamatergic transmission in these areas as well. This hypothesis is consistent with the increased anxiety-like behavior following ethanol exposure/withdrawal (Lack et al., 2007). Likewise, the alcohol-dependent recruitment of mechanisms responsible for the expression of synaptic plasticity in the BLA is
