Citation

Luo H, Pace E, Zhang X, Zhang J. Neurosci. Lett. 2014; 580: 47-51.

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 © 2014, Elsevier Publishing)

DOI

10.1016/j.neulet.2014.07.041

PMID

25092609

Abstract

High-pressure blast shockwaves are known to cause tinnitus. Imaging studies have shown that blast-induced tinnitus may result from damage to the inner ear structures and/or direct brain impact that trigger a cascade of neuroplastic changes in both auditory and non-auditory centers. Nevertheless, information is still lacking on the neurophysiological mechanisms underlying blast-induced tinnitus. In this study, we used a rat model and investigated the effect of blast-induced tinnitus on spontaneous activity in the inferior colliculus (IC) at one day, one month, and three months following blast. Our results showed that rats with behavioral evidence of tinnitus exhibited hyperactivity in all frequency regions at one day post-blast. Although the induced hyperactivity persisted throughout a three-month recording period, it was more robust in middle-frequency loci at one month after blast exposure and in middle-to-high-frequency loci at three months after blast. Our results also showed increased bursting rate in the low and middle frequency regions at one day after blast, in the middle frequency region at one month after blast, and in all frequency regions at three months after blast. The findings suggest that neuroplasticity as reflected by shifted tonotopic representations of hyperactivity and bursting activity subserves blast-induced tinnitus and hearing impairment.

Language: en