The amygdala formation is implicated in generation of emotional states such as anxiety and fear. Many substances that modulate neuronal activity in the amygdala alter anxiety. Cholecystokinin (CCK) is an endogenous neuropeptide that induces anxiety states in behavioral studies in both animals and humans. Using a brain slice preparation, we found that application of CCK increases inhibitory synaptic transmission measured in projection neurons of the basolateral amygdala. To determine the source of the increased inhibition we examined the direct effect of CCK on local interneurons in this region. CCK most strongly depolarized fast-spiking interneurons. Burst-firing and regular-firing interneurons were also depolarized, although to a lesser degree. However, another distinct group of interneurons was unaffected by CCK. These effects were mediated by the CCKB receptor subtype. The excitatory effect of CCK appeared to be mediated by both a nonselective cation and a K+ current.