Withdrawal anxiety is a significant factor contributing to continued alcohol abuse in alcoholics. This anxiety is extensive, long-lasting, and develops well after the obvious physical symptoms of acute withdrawal. The neurobiological mechanisms underlying this prolonged withdrawal-induced anxiety are not well understood. The basolateral amygdala is a major emotional center in the brain and regulates the expression of anxiety. New evidence suggests that increased glutamatergic function in the basolateral amygdala may contribute to withdrawal-related anxiety following chronic ethanol exposure. Recent evidence also suggests that kainate-type ionotropic glutamate receptors are inhibited by intoxicating concentrations of acute ethanol. This acute sensitivity suggests potential contributions by these receptors to the increased glutamatergic function seen during chronic exposure. Therefore we examined the effect of chronic intermittent ethanol (CIE) and withdrawal (WD) on kainate receptor (KAR) mediated synaptic transmission in the basolateral amygdala (BLA) of Sprague Dawley rats. Our study showed that CIE, but not withdrawal, increased synaptic responses mediated by KARs. Interestingly, both CIE and WD occluded KAR-mediated synaptic plasticity. Finally, we found that BLA fEPSP responses were increased during CIE and WD via a mechanism that is independent from glutamate release from presynaptic terminals. Taken together, these data suggest that KARs might also contribute to postsynaptic increases in glutamatergic synaptic transmission during CIE and that the mechanisms responsible for the expression of KAR-dependent synaptic plasticity might be engaged by chronic ethanol exposure and withdrawal.