한빛사논문
Abstract
Sungchil Yanga, Benjamin D. Weinera, Li S. Zhanga, Sung-Jin Chob, and Shaowen Baoa,1
aHelen Wills Neuroscience Institute and
bDepartment of Molecular and Cell Biology, University of California, Berkeley, CA 94720
Edited* by Michael M. Merzenich, Brain Plasticity, Inc., San Francisco, CA, and approved August 2, 2011 (received for review May 19, 2011)
Abstract
Hearing loss often results in tinnitus and auditory cortical map changes, leading to the prevailing view that the phantom perception is associated with cortical reorganization. However, we show here that tinnitus is mediated by a cortical area lacking map reorganization. High-frequency hearing loss results in two distinct cortical regions: a sensory-deprived region characterized by a decrease in inhibitory synaptic transmission and a normal hearing region showing increases in inhibitory and excitatory transmission and map reorganization. Hearing-lesioned animals displayed tinnitus with a pitch in the hearing loss range. Furthermore, drugs that enhance inhibition, but not those that reduce excitation, reversibly eliminated the tinnitus behavior. These results suggest that sensory deprivation-induced homeostatic down-regulation of inhibitory synapses may contribute to tinnitus perception. Enhancing sensory input through map reorganization may plausibly alleviate phantom sensation.
auditory cortex, GABA, phantom pain, tonic inhibitiondeafness
Footnotes
1To whom correspondence should be addressed.
Author contributions: S.Y., B.D.W., and S.B. designed research; S.Y., B.D.W., L.S.Z., and S.-J.C. performed research; S.Y., B.D.W., and S.-J.C. contributed new reagents/analytic tools; S.Y., B.D.W., L.S.Z., and S.B. analyzed data; and S.Y. and S.B. wrote the paper.
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