Cochlear function and audiogenic seizures: developmental covariance in the LP/J mouse.
Innate susceptibility to audiogenic seizures develops and declines at varying rates and ages, depending upon genotype and environmental conditions. Auditory dysfunctions have been experimentally produced which induce susceptibility in otherwise nonsusceptible mouse strains. In order to more closely correlate cochlear functions and audiogenic seizures in genetically susceptible mice, both measures were obtained from LP/J mice, at ages ranging from 8 to 120 days. Susceptibility to sound-produced convulsions was first noted at 12 days, was maximal from 18 to 32 days, declined rapidly by 40 days, and disappeared by 120 days of age. Cochlear nerve-evoked potential thresholds were very high at 12 days, were lowest between 18 and 32 days and increased thereafter. The correlation between susceptibility and cochlear thresholds was greatest for high frequencies (r = -.93), intermediate for midfrequency (r = -.77), and poorest for low frequencies (r = -.56). It was concluded that either genetic or environmental factors which produce an intermediate level of high frequency cochlear damage in the young mouse will produce susceptibility to audiogenic seizures.
D000161:Acoustic Stimulation; D000818:Animals; D001309:Auditory Threshold; D003051:Cochlea / Q000503:physiopathology*; D003056:Cochlear Nerve / Q000503:physiopathology; D004198:Disease Susceptibility; D051379:Mice; D008815:Mice, Inbred Strains; D012640:Seizures / Q000235:genetics / Q000503:physiopathology*