Mice heterozygous for the Serpinb6a null mutation show deficits in central auditory function after acoustic trauma

Objectives Complete deficiency of the serine protease inhibitor gene, SERPINB6, is responsible for autosomal-recessive, nonsyndromic sensorineural hearing loss in humans. A mouse model of this deafness gene identifies Serpinb6a expression in the neurosensory epithelium and fibrocytes of the cochlea. Homozygous Serpinb6a mutant mice display an exaggerated hearing loss after exposure to moderate acoustic trauma. It is unknown if and how heterozygous Serpinb6a mice show increased vulnerability to acoustic trauma. Methods We exposed Serpinb6a+/− and Serpinb6a+/+ mice to acoustic trauma and measured their hearing function prior to, 3 and 14 days postexposure, analysing shifts in hearing threshold and amplitudes of Wave I and II of the auditory brainstem-evoked response (ABR) to 4, 8, 16 and 32 kHz tones. Results Shifts in hearing threshold and Wave I amplitude of Serpinb6a+/− mice were not significantly different from Serpinb6a+/+ mice at both time points and all frequencies tested (P > 0.05, Mann–Whitney test). However, Wave II amplitudes at 16 and 32 kHz tones, were more severely diminished in Serpinb6a+/− mice (P 
Source: NeuroReport - Category: Neurology Tags: Integrative Systems Source Type: research