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 also consistent with the attenuation of amygdala-dependent fear learning following multiple withdrawals (Stephens et al., 2001). The present findings illustrate additional neurophysiological mechanisms by which chronic ethanol and withdrawal influence anxiety-related neural circuitry.
