Withdrawal anxiety is a significant factor contributing to continued alcohol abuse in alcoholics. This anxiety is long lasting, can manifest well after the overt physical symptoms of withdrawal, and is frequently associated with relapse in recovering alcoholics. The neurobiological mechanisms governing these withdrawal-associated increases in anxiety are currently unknown. The basolateral amygdala is a major emotional center in the brain and regulates the expression of both learned-fear and anxiety. Neurotransmitter system alterations within this brain region may therefore contribute to withdrawal-associated anxiety. Since evidence suggests that glutamate-gated neurotransmitter receptors are sensitive to acute ethanol exposure, we examined the effect of chronic intermittent ethanol (CIE) and withdrawal (WD) on glutamatergic synaptic transmission in the basolateral amygdala. We found that slices prepared from CIE and WD animals had significantly increased contributions by synaptic NMDA-receptors. In addition, CIE increased the amplitude of AMPA receptor-mediated spontaneous excitatory postsynaptic currents (sEPSC), while only WD altered the amplitude and kinetics of tetrodotoxin-resistant spontaneous events (mEPSC). Similarly, the frequency of sEPSCs was increased in both CIE and WD neurons; but, only WD increased the frequency of mEPSCs. These data suggest that CIE and WD differentially alter both pre- and post-synaptic properties of BLA glutamatergic synapses. We also show that microinjection of the AMPA receptor antagonist, DNQX, can attenuate withdrawal-related anxiety-like behavior. Together, our results suggest that the increased glutamatergic function may contribute to anxiety expressed during withdrawal from chronic ethanol.