Growing evidence has been found to suggest that early development of the central auditory system is dependent on acoustic stimuli. Peripheral damage caused by noise exposure and ototoxic drugs can induce functional an...Growing evidence has been found to suggest that early development of the central auditory system is dependent on acoustic stimuli. Peripheral damage caused by noise exposure and ototoxic drugs can induce functional and anatomical changes along the auditory pathways. The inferior colliculus (IC) is a unique structure in the auditory system located between the primary auditory nuclei of the brainstem and the thala-mus. Damage to the IC inhibitory circuitry may affect central auditory processing and sound perception. Here, we review some of the striking electrophysiological changes in the IC that occur after noise exposure and ototoxic drug treatment. A common occurrence that emerges in the IC after peripheral damage is hyper-excitability of sound-evoked response. The hyperexcitability of the IC is likely related with reduced inhibi-tory response that requires normal peripheral inputs. Early age hearing loss can result in a long lasting in-creased susceptibility to audiogenic seizure which is related to hyperactivity in the IC evoked by loud sounds. Our studies suggest that hearing loss can cause increased IC neuron responsiveness which may be related to tinnitus, hyperacusis, and audiogenic seizure.展开更多
基金supported by Royal National Institute for Deaf People
文摘Growing evidence has been found to suggest that early development of the central auditory system is dependent on acoustic stimuli. Peripheral damage caused by noise exposure and ototoxic drugs can induce functional and anatomical changes along the auditory pathways. The inferior colliculus (IC) is a unique structure in the auditory system located between the primary auditory nuclei of the brainstem and the thala-mus. Damage to the IC inhibitory circuitry may affect central auditory processing and sound perception. Here, we review some of the striking electrophysiological changes in the IC that occur after noise exposure and ototoxic drug treatment. A common occurrence that emerges in the IC after peripheral damage is hyper-excitability of sound-evoked response. The hyperexcitability of the IC is likely related with reduced inhibi-tory response that requires normal peripheral inputs. Early age hearing loss can result in a long lasting in-creased susceptibility to audiogenic seizure which is related to hyperactivity in the IC evoked by loud sounds. Our studies suggest that hearing loss can cause increased IC neuron responsiveness which may be related to tinnitus, hyperacusis, and audiogenic seizure.
