Citation

Luo H, Pace E, Zhang J. Neuroscience 2016; 340: 515-520.

Affiliation

Department of Otolaryngology-Head and Neck Surgery, Wayne State University School of Medicine, Detroit, Michigan; Department of Communication Sciences & Disorders, Wayne State University College of Liberal Arts & Sciences, Detroit, Michigan. Electronic address: jinzhang@med.wayne.edu.

Copyright

(Copyright © 2016, International Brain Research Organization, Publisher Elsevier Publishing)

DOI

10.1016/j.neuroscience.2016.11.014

PMID

27865868

Abstract

Blast exposure can cause tinnitus and hearing impairment by damaging the auditory periphery and direct impact to the brain, which trigger neural plasticity in both auditory and non-auditory centers. However, the underlying neurophysiological mechanisms of blast-induced tinnitus are still unknown. In this study, we induced tinnitus in rats using blast exposure and investigated changes in spontaneous firing and bursting activity in the auditory cortex at one day, one month, and three months after blast exposure. Our results showed that spontaneous activity in the tinnitus positive group began changing at one month after blast exposure, and manifested as robust hyperactivity at all frequency regions at three months after exposure. We also observed an increased bursting rate in the low frequency region at one month after blast exposure and in all frequency regions at three months after exposure. Taken together, spontaneous firing and bursting activity in the auditory cortex played an important role in blast-induced chronic tinnitus as opposed to acute tinnitus, thus favoring a bottom-up mechanism.

Copyright © 2016 IBRO. Published by Elsevier Ltd. All rights reserved.

Language: en