Neonatal cochlear hearing loss results in developmental abnormalities of the central auditory pathways.
We have used animal models of long term neonatal cochlear hearing loss to study developmental plasticity of the central auditory pathways. Newborn chinchilla pups and feline kittens were treated with the ototoxic drug amikacin, so as to induce basal lesions in the cochlea. At maturity these animals were used in single unit electrophysiological mapping studies, in which the cochleotopic organization of primary auditory cortex (of the cat) and the inferior colliculus of the midbrain (in the chinchilla) were mapped. We have observed, both in the midbrain and auditory cortex, massive reorganization of frequency representation. Most striking were the presence of large monotonic regions (i.e. large areas in which all neurons have similar tuning properties). Cochlear lesions which involve inner hair cells clearly modify the normal development of cochleotopic representation in the midbrain and cortical regions. We suggest that similar abnormal patterns of frequency representation will exist in human subjects with long term neonatal hearing loss.
Department of Otolaryngology, Hospital for Sick Children, Toronto, Canada.
R V
RV
Harrison
S G
SG
Stanton
D
D
Ibrahim
A
A
Nagasawa
R J
RJ
Mount
D000583:Amikacin; D000818:Animals; D000831:Animals, Newborn; D001303:Auditory Cortex / Q000473:pathology* / Q000503:physiopathology; D001306:Auditory Pathways / Q000473:pathology*; D002415:Cats; D002682:Chinchilla; D015834:Cochlear Diseases / Q000139:chemically induced / Q000150:complications*; D006199:Hair Cells, Auditory, Inner / Q000187:drug effects; D006314:Hearing Loss, Conductive / Q000139:chemically induced / Q000503:physiopathology*; D007245:Inferior Colliculi / Q000473:pathology* / Q000503:physiopathology
D000583:Amikacin