Abstract
An acquired audiogenic seizure model was created in rats by exposing them to intense 1/3 octave band noise (4 kHz, 125 dB) delivered two times, on post-natal days (P) 14 and 28. On P 28, “wild-running” (WR) was induced by sound in rats which had been formerly exposed to the sound stimulus on P 14. In stimulated rats and/or those with seizures, changes in auditory brainstem response (ABR) were characterized by a rise in the sound level threshold, indicative of cochlear hearing impairment, a decrease in the amplitude ratio of waves II and III to wave I, and prolongation of the interpeak latency between waves I and IV.
In the rats with seizures, many cells showing Fos-like immuno-reactivity were found in the lateral lemniscus, inferior colliculus, medial geniculate body, and temporal cortex, and the nerve cells in these nuclei showed slight histopathological change.
The central part of the inferior colliculus which is critical for initiation of audiogenic seizure is not expressed in non wild running rats, suggesting that activation of this area by a single audiogenic seizure is not sufficient to induce long-lasting changes. Strong acoustic stimuli induce an abnormal response in the inferior colliculus, accompanied by a wild running phase. These results confirm that audiogenic seizures are brain-stem seizures relatred to dysfunction of auditory pathways.
