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Early age conductive hearing loss causes audiogenic seizure and hyperacusis behavior - PubMed

Early age conductive hearing loss causes audiogenic seizure and hyperacusis behavior

Wei Sun et al. Hear Res. 2011 Dec.

Abstract

Recent clinical reports found a high incidence of recurrent otitis media in children suffering hyperacusis, a marked intolerance to an otherwise ordinary environmental sound. However, it is unclear whether the conductive hearing loss caused by otitis media in early age will affect sound tolerance later in life. Thus, we have tested the effects of tympanic membrane (TM) damage at an early age on sound perception development in rats. Two weeks after the TM perforation, more than 80% of the rats showed audiogenic seizure (AGS) when exposed to loud sound (120 dB SPL white noise, < 1 min). The susceptibility of AGS lasted at least sixteen weeks after the TM damage, even the hearing loss recovered. The TM damaged rats also showed significantly enhanced acoustic startle responses compared to the rats without TM damage. These results suggest that early age conductive hearing loss may cause an impaired sound tolerance during development. In addition, the AGS can be suppressed by the treatment of vigabatrin, acute injections (250 mg/kg) or oral intakes (60 mg/kg/day for 7 days), an antiepileptic drug that inhibits the catabolism of GABA. c-Fos staining showed a strong staining in the inferior colliculus (IC) in the TM damaged rats, not in the control rats, after exposed to loud sound, indicating a hyper-excitability in the IC during AGS. These results indicate that early age conductive hearing loss can impair sound tolerance by reducing GABA inhibition in the IC, which may be related to hyperacusis seen in children with otitis media.

Published by Elsevier B.V.

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Figures

Figure 1
Figure 1

Early age tympanic membrane damage induced hearing loss and audiogenic seizure (AGS). A. Tympanic membrane (TM) damage caused a 10 to 30 dB hearing threshold increase compared to the Control Group two weeks after the surgery. B. The differences of the hearing threshold between the TM Group and the Control Group reduced to 10-15 dB six weeks after the TM damage (Results are presented as mean ± SEM)

Figure 2
Figure 2

Tympanic membrane (TM) damage caused increased acoustic startle response. A. Rats with TM damage showed higher acoustic startle response at 4 kHz (Two-way ANOVA, p = 0.004, F(1,36)= 9.38, n = 4) compared to the Control Group. B. At 8 kHz, the startle responses of the TM Group were higher at 100 and 110 dB SPL, but slightly lower from 70 to 90 dB SPL compared to the Control Group (Results are presented as mean ± SEM, * P < 0.05).

Figure 3
Figure 3

The c-Fos staining in the inferior colliculus in a control rat (A and C) and a tympanic membrane (TM) damaged rat (B and D). The inferior colliculus tissue was harvested 2 hours after exposure to 120 dB SPL white noise (1 minute). A strong c-Fos staining can be seen in the TM damaged rats primarily in the external nuclei (ECIC), the dorsal nuclei (DCIC) and the central nuclei of the inferior colliculus (CIC) (B and D), not in the rat in the Control Group (A and C).

Figure 4
Figure 4

Oral treatment of vigabatrin (60 mg/kg/day, seven days) did not affect the acoustic startle response. Acoustic startle responses were tested in adult rats with TM damage at early age before and after vigabatrin treatment at (A) 4 kHz and (B) 8 kHz. There was no significant different before and after the treatment (n = 4, two-way ANOVA, P>0.05) (Results are presented as mean ± SEM).

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