کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6257132 | 1612946 | 2015 | 10 صفحه PDF | دانلود رایگان |
- Early noise exposure on P14 elicited transient hyper-reactivity for 2 weeks.
- Startle responses in exposed rats had decreased thresholds and increase amplitudes.
- The number of ribbon synapses, but not hair cells, decreased significantly.
- Altered startle responses persisted into adulthood even in rats with normal thresholds.
Even brief acoustic trauma during the critical period of development that results in no permanent hearing threshold shift may lead to altered auditory processing in adulthood. By monitoring the acoustic startle response (ASR), we examined the development of auditory function in control rats and in rats exposed to intense noise at the 14th postnatal day (P14). First ASRs appeared on P10-P11 to intense low-frequency tones. By P14, the range of sound intensities and frequencies eliciting ASRs extended considerably, the ASR reactivity being similar at all frequencies (4-32Â kHz). During the subsequent two weeks, ASR amplitudes to low-frequency stimuli (4-8Â kHz) increased, whereas the ASRs to high-frequency tones were maintained (16Â kHz) or even decreased (32Â kHz). Compared to controls, noise exposure on P14 (125Â dB SPL for 8, 12, or 25Â min) produced transient hyper-reactivity to startle stimuli, manifested by a decrease of ASR thresholds and an increase of ASR amplitudes. ASR enhancement occurred regardless of permanent hearing loss and was more pronounced at high frequencies. The hyper-reactivity of ASRs declined by P30; the ASR amplitudes in adult exposed rats were lower than in controls. The histological control did not reveal loss of hair cells in adult exposed rats, however, the number of inner hair cell ribbon synapses was significantly decreased, especially in the high-frequency part of the cochlea. The results indicate that early acoustic trauma may result in complex changes of ASRs during development.
Journal: Behavioural Brain Research - Volume 286, 1 June 2015, Pages 212-221