Abstract
Animal models continue to improve our understanding of tinnitus pathogenesis and aid in development of new treatments. However, there are no diagnostic biomarkers for tinnitus-related pathophysiology for use in awake, freely moving animals. To address this disparity, two complementary methods were combined to examine reliable tinnitus models (rats repeatedly administered salicylate or exposed to a single noise event): inhibition of acoustic startle and manganese-enhanced MRI. Salicylate-induced tinnitus resulted in wide spread supernormal manganese uptake compared to noise-induced tinnitus. Neither model demonstrated significant differences in the auditory cortex. Only in the dorsal cortex of the inferior colliculus (DCIC) did both models exhibit supernormal uptake. Therefore, abnormal membrane depolarization in the DCIC appears to be important in tinnitus-mediated activity. Our results provide the foundation for future studies correlating the severity and longevity of tinnitus with hearing loss and neuronal activity in specific brain regions and tools for evaluating treatment efficacy across paradigms.
Highlights
Tinnitus, the perception of a ringing, buzzing, or hissing in the absence of an external stimulus due to noise, drugs, or traumatic brain injury, is a rapidly growing major health concern affecting both civilian and military populations [1,2,3,4]
Sub-divisions of the inferior colliculus besides the dorsal cortex of the inferior colliculus (DCIC) failed to reach statistical significance (Figure 8), we found no evidence for groupwise regional differences within the inferior colliculus: Tests for both the ECIC and CNIC regions reached marginal significance, and showed a similar between-group pattern of manganese uptake (Figure 8 i.e. control,salicylate; noise
Using this approach we found that both salicylate and noise-induced tinnitus result in increased neuronal activity in DCIC neurons
Summary
The perception of a ringing, buzzing, or hissing in the absence of an external stimulus due to noise, drugs, or traumatic brain injury, is a rapidly growing major health concern affecting both civilian and military populations [1,2,3,4]. Mounting evidence suggests that tinnitus can be linked with increased spontaneous neuronal activity [5,6,7,8] leading to the use of drugs targeted at reducing spikes of increased activity. Such approaches have only been partially successful [5,9,10,11,12]. There is a pressing need to analytically measure calcium ion regulation in auditory-related brain regions to determine whether or not common brain regions and abnormalities exist across tinnitus models
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