Fos-immunoreactive responses in inferior colliculi of rats with experimental audiogenic seizure susceptibility.

Abstract

Audiogenic seizure (AGS) susceptibility is a reflex epilepsy of rodents in which acoustic stimulation evokes wild running attacks and subsequent convulsions. Susceptibility can be induced in non-susceptible strains by treatments causing transient or permanent hearing losses as long as these occur during the neonatal period. The defect which is the basis of susceptibility has been proposed to be a failure of developmental organization of inferior colliculus (IC) into frequency selective zones. That is, high frequency stimuli evoke responses in broader arrays of neurons in ICs of susceptible rats than in those of neonatally untreated (non-susceptible) controls. Nonetheless, this observation has been made only in rats in which susceptibility was induced by exposure to intense noise on postnatal day (PND) 14. By contrast, the present study examines whether unusually broad topographic responses are also characteristic in ICs of rats made susceptible by the neonatal administration of low doses of the ototoxic antibiotic, kanamycin (KM). Patterns of Fos-like immunoreactivity (Foslir) induced by seizures or pure tone stimuli were compared in ICs of adult Wistar rats which neonatally had been (a) sham-treated; (b) noise-exposed on PND 14; or (c) injected on PNDs 9-12 with 100 mg/kg KM. It was found that sound-triggered seizures in the two experimental groups resulted in induction of Foslir primarily within cortical areas of IC. By contrast, pure tones evoked unusually broad responses in the central nucleus of ICs of both susceptible groups but not in those of controls. Additionally, in the KM-treated rats, the range of frequencies evoking abnormal responses extended one octave lower than was characteristic of noise-exposed rats. The earlier schedule of treatments in the KM model may account for this inasmuch as low frequency response domains undergo development at younger ages. The similarity of results in the two models suggests failure of development of frequency selective fields in IC is indeed the common basis of experimentally induced susceptibility to sound-triggered seizures.