Hearing research · 2022
Ipsilateral auditory cortex responses to the intact ear after unilateral noise trauma in juvenile rats.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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Jiang Chen, Luo Bin, Liu Xiaopeng, Chen Guang-Di, Salvi Richard
Аннотация
BACKGROUND: While ear stimulation produces a robust response in the contralateral auditory cortex (AC), it produces only a weak response in the ipsilateral AC, known as interhemispheric asymmetry. Unilateral deafness can lead to AC plastic changes, resulting in reduced interhemispheric asymmetry and auditory perceptual consequences. However, the unilateral hearing loss-associated plastic changes are far from fully understood. The purpose of this study was to investigate AC responses to the ipsilateral unimpaired ear after noise injury to the contralateral ear in juvenile rats.
METHODS: Rats (50 days) were monaurally exposed to an intense noise (10.0-12.5 kHz, 126 dB SPL) for 2 hours. The unexposed ear-induced ipsilateral AC responses were recorded 2 days and 4 months after exposure and compared between groups.
RESULTS: The noise exposure resulted in complete hearing loss in the exposed ear, but normal function in the other. Two days after exposure, the ipsilateral AC response induced by the intact ear was significantly enhanced and the threshold decreased (the early-onset effect). Four months after noise exposure, in addition to the increased response amplitude, the "slow-increasing" firing pattern of the neurons in the ipsilateral AC turned into the contralateral-AC-response-like "sharp-increasing" pattern (the late-onset effect) with shortened response latency.
DISCUSSION: The early-onset effect can result from release of inhibition due to decreased contralateral input, while the late-onset effect may imply the formation of direct connections in the ipsilateral auditory pathway. The enhanced AC response may help maintain loudness perception and monaural sound localization after unilateral deafness.
METHODS: Rats (50 days) were monaurally exposed to an intense noise (10.0-12.5 kHz, 126 dB SPL) for 2 hours. The unexposed ear-induced ipsilateral AC responses were recorded 2 days and 4 months after exposure and compared between groups.
RESULTS: The noise exposure resulted in complete hearing loss in the exposed ear, but normal function in the other. Two days after exposure, the ipsilateral AC response induced by the intact ear was significantly enhanced and the threshold decreased (the early-onset effect). Four months after noise exposure, in addition to the increased response amplitude, the "slow-increasing" firing pattern of the neurons in the ipsilateral AC turned into the contralateral-AC-response-like "sharp-increasing" pattern (the late-onset effect) with shortened response latency.
DISCUSSION: The early-onset effect can result from release of inhibition due to decreased contralateral input, while the late-onset effect may imply the formation of direct connections in the ipsilateral auditory pathway. The enhanced AC response may help maintain loudness perception and monaural sound localization after unilateral deafness.