Plasticity at glutamatergic synapses is believed to be the cellular correlate of learning and memory. Classic fear conditioning, for example, is dependent upon NMDA-type glutamate receptor activation in the lateral/basolateral amygdala followed by increased synaptic expression of AMPA-type glutamate receptors. This review provides an extensive comparison between the initiation and expression of glutamatergic plasticity during learning/memory and glutamatergic alterations associated with chronic ethanol exposure and withdrawal. The parallels between these neuro-adaptive processes suggest that long-term ethanol exposure might "chemically condition" amygdala-dependent fear/anxiety via the increased function of pre- and post-synaptic glutamate signaling.
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