An impressive amount of evidence from many different laboratories using a variety of experimental techniques indicates that the amygdala plays a crucial role in the acquisition, consolidation and retention or expression of conditioned fear. Electrophysiological data are beginning to detail the transmitters and inter-amygdala connections that transmit information to, within, and out of the amygdala. In general, treatments that increase the excitability of amygdala output neurons in the basolateral nucleus (for example, by decreasing opiate and GABA transmission, and increasing noradrenergic transmission) improve aversive conditioning, whereas treatments that decrease excitability of these neurons (by increasing opiate and GABA transmission, and decreasing NMDA and noradrenergic transmission) retard aversive conditioning as well as producing anxiolytic effects in appropriate animal tests. A better understanding of brain systems that inhibit the amygdala, as well as the role of its very high levels of peptides, might eventually lead to the development of more effective pharmacological strategies for treating clinical anxiety and memory disorders.