Susceptibility to audiogenic seizures has been produced in otherwise non-susceptible mice by acoustic stress and by conductive hearing loss. Both procedures temporarily elevate the absolute threshold of the auditory evoked potential (AEP) and are maximally effective during a circumscribed period of early development. In the genetically SUSCEPTIBLE DBA/2J mouse, AEP thresholds indicated that its auditory system is functionally less mature during this early period than that of the nonsusceptible C57BL/6Jmouse. It was proposed that innate susceptibility found in the DBA/2J mouse results from auditory disuse supersensitivity during a critical developmental period, in support of Saunders' hypothesis for acoustically primed mice. The increased peak-to-peak AEP amplitudes, however, were not believed to be causally related to the audiogenic seizures.