Area-dependent change of response in the rat’s inferior colliculus to intracochlear electrical stimulation following neonatal cochlear damage

• Published in: Scientific reports 2019-04, Vol.9 (1), p.5643-5643, Article 5643
• Main Authors: Hatano, Miyako, Kelly, Jack B., Zhang, Huiming
• Format: Article
• Language: English
• Subjects: 631/378/1689/2608; 631/378/1697/2602; 631/378/2619/1387; 631/378/2619/1639; 631/378/3917; 9/30; Acoustic Stimulation - methods; Amikacin; Amikacin - pharmacology; Animals; Brain injury; Cochlea; Cochlea - physiology; Cochlear Implants; Deafness - physiopathology; Electric Stimulation - methods; Electrical stimuli; Evoked Potentials, Auditory, Brain Stem; Female; Ganglion cells; Geographical variations; Hair; Hair cells; Hair Cells, Auditory - physiology; Humanities and Social Sciences; Inferior Colliculi - physiology; Inferior colliculus; Male; Mesencephalon; multidisciplinary; Neonates; Neurons - physiology; Owls; Rats; Rats, Wistar; Science; Science (multidisciplinary); Sensory deprivation; Spiral ganglion; Spiral Ganglion - physiology
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-019-41955-y

To understand brain changes caused by auditory sensory deprivation, we recorded local-field potentials in the inferior colliculus of young adult rats with neonatal cochlear damage produced by systemic injections of amikacin. The responses were elicited by electrical stimulation of the entire cochlea and recorded at various locations along a dorsolateral-ventromedial axis of the inferior colliculus. We found that hair cells were completely destroyed and spiral ganglion neurons were severely damaged in the basal cochleae of amikacin-treated animals. Hair cells as well as spiral ganglion neurons were damaged also in the middle and apical areas of the cochlea, with the damage being greater in the middle than the apical area. Amplitudes of local-field potentials were reduced in the ventromedial inferior colliculus, but enhanced in the dorsolateral inferior colliculus. Latencies of responses were increased over the entire structure. The enhancement of responses in the dorsolateral inferior colliculus was in contrast with the damage of hair cells and spiral ganglion cells in the apical part of the cochlea. This contrast along with the overall increase of latencies suggests that early cochlear damage can alter neural mechanisms within the inferior colliculus and/or the inputs to this midbrain structure.