The inferior colliculus (IC) is established as the initiation site within the neuronal network for audiogenic seizures (AGS), but the relative importance of the IC subnuclei in AGS is controversial. The lateral and basolateral subdivisions of the amygdala are implicated in the expansion of the AGS network that occurs during AGS kindling. However, the role of the amygdala in the AGS network in nonkindled AGS is unknown. NMDA receptors are implicated in modulation of AGS and in neurotransmission in both the IC and amygdala. Therefore, changes in AGS severity in genetically epilepsy-prone rats (GEPR-9s) were examined after bilateral focal microinjection into IC subnuclei or lateral/basolateral subdivisions of the amygdala of a competitive NMDA receptor antagonist, 3-((+)-2-carboxypiperazine-4-yl)propyl-1-phosphonic acid (CPP). Blockade of AGS in IC central nucleus (ICc) and external cortex (ICx) was observed at identical doses of CPP, but these doses were ineffective in IC dorsal cortex (ICd). Microinjection of CPP into the amygdala did not produce significant changes in AGS severity except at doses 20 times those effective in IC. The latter data contrast with the anticonvulsant effects of amygdala microinjections on seizure severity in kindled AGS reported previously. The present data in concord with neuronal recording studies of these nuclei suggest that the ICc is the most critical site in AGS initiation, the ICx in propagation, and that the ICd plays a lesser role in the AGS network. The amygdala does not appear to play a requisite role in the neuronal network for AGS in animals that have not been subjected to AGS kindling.