Effect of priming and tympanic membrane destruction on development of audiogenic seizure susceptibility in BALBc mice

Chen, Chia-Shong; Gates, G. Richard; Bock, Gregory R.

doi:10.1016/0014-4886(73)90230-6

Cited by 44 publications

(12 citation statements)

References 15 publications

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“…Evidence is accumulating that exposure to intense noise for a brief period of time results in at least 2, and perhaps more, physiological defense responses in these mice. First, peripheral responses are activated as indicated by the phenomenon o f unilateral priming (Chen, Gates, & Bock, 1973;Fuller & Collins, 1968). Other evidence for a peripheral involvement comes from data which indicate temporary threshold shifts-a raised auditory threshold with an as yet undetermined time course-which been taken as presumptive evidence of altered hearing in these mice (Henry, 1972;Saunders, Bock, Chen, & Gates, 1972;Saunders, Bock, James, & Chen, 1972).…”

Section: Discussionmentioning

confidence: 99%

Effects of stimulus intensity and stimulus duration during acoustic priming on audiogenic seizures in C57BL/6J mice

Schreiber

1977

Developmental Psychobiology

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The effects of stimulus intensity and stimulus duration were examined in C57BL/6J mice not susceptible to audiogenic seizures (AGS) on the 1st exposure to an acoustic stimulus. Two experiments were performed. In the 1st, 16-day-old mice were exposed to 108, 112, 120, or 127 dB for 60 sec. Mice were then tested for susceptibility to AGS at varying ages thereafter. Increasing intensity of noise during priming resulted in heightened peak seizure risk, and extended duration of peak seizure risk, and a prolonged time of seizure risk. In the 2nd experiment, mice were exposed for 5, 15, 30, or 60 sec to 127 dB of noise. Five seconds of noise was barely sufficient to induce later susceptibility to AGS. Increasing stimulus duration from 15 to 30 to 60 sec resulted in increasing seizure risk and duration of peak risk period.

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Section: Discussionmentioning

confidence: 99%

Effects of stimulus intensity and stimulus duration during acoustic priming on audiogenic seizures in C57BL/6J mice

Schreiber

1977

Developmental Psychobiology

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“…Previous animal studies have shown that early age conductive hearing loss can impair sound tolerance (Chen et al, 1973; Gates et al, 1973; McGinn et al, 1973). Chen et al reported that a high incidence of audiogenic seizure (AGS) behavior was induced in mice by rupturing their tympanic membranes (TM) at an early age (postnatal 14 or 21 days), but not in adult (Chen et al, 1973).…”

Section: Introductionmentioning

confidence: 99%

“…Chen et al reported that a high incidence of audiogenic seizure (AGS) behavior was induced in mice by rupturing their tympanic membranes (TM) at an early age (postnatal 14 or 21 days), but not in adult (Chen et al, 1973). During exposure to loud sound, i.e., ringing bells for 120 seconds (~125 dB SPL), the TM damaged mice exhibited wild running followed by erratic leaping, clonic convulsion and even death.…”

Section: Introductionmentioning

confidence: 99%

Early age conductive hearing loss causes audiogenic seizure and hyperacusis behavior

et al. 2011

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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 minute). 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.

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“…The percentage of subjects displaying AGS behaviors when tested on other days was reduced. Similarly, in the sound-deprivation paradigm, Chen et al (1973) found that subjects with tympanic membranes destroyed on postnatal Day 14 were more susceptible to AGS than subjects with tympanic membranes destroyed on Day 21. Therefore, manipulation of acoustic stimulus parameters within a specific period of development may alter responsiveness to subsequent exposure to intense sound.…”

mentioning

confidence: 94%

Audiogenic seizures in the developmentally primed Long-Evans rat

Ross

Coleman

1999

Dev. Psychobiol.

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Effect of priming and tympanic membrane destruction on development of audiogenic seizure susceptibility in BALBc mice

Cited by 44 publications

References 15 publications

Effects of stimulus intensity and stimulus duration during acoustic priming on audiogenic seizures in C57BL/6J mice

Effects of stimulus intensity and stimulus duration during acoustic priming on audiogenic seizures in C57BL/6J mice

Early age conductive hearing loss causes audiogenic seizure and hyperacusis behavior

Audiogenic seizures in the developmentally primed Long-Evans rat

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