![]() ![]() If the gap is embedded in a tone that closely matches the animal's tinnitus in frequency and intensity, the result is a full startle reflex that is not blunted. If the pre-stimulus gap is detected, there is a decreased startle reflex observed when the startle stimulus is presented ( Figure 1A–B). The paradigm was designed to assess whether the subject perceives tinnitus by introducing a pre-stimulus “gap” in sound (silence) just prior to the startle stimulus. Despite such promising results, 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.Ī recent methodological advance in the tinnitus field involves the use of gap and pre-pulse inhibition of the acoustic startle reflex (ASR) for screening of tinnitus percepts in animal models. Blocking calcium channels with nimodipine has been shown to reduce percepts associated with salicylate-induced tinnitus,. A better understanding of the pathophysiology of tinnitus is needed to improve future treatment efforts.Īnimal models of tinnitus (e.g., noise or drug induced) produce increases in spontaneous neuronal activity, which are likely downstream consequences of changes in calcium and calcium channel-dependent neurotransmitter release. However, such approaches have only been partially successful, ,. Mounting evidence suggests that tinnitus can be linked with increased spontaneous neuronal activity, ,, leading to the use of drugs targeted at reducing spikes of increased activity. 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,. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: The authors have declared that no competing interests exist. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.įunding: These studies were supported by the National Institutes of Health, University Medical Student Grant to GR, an unrestricted grant from Research to Prevent Blindness (Kresge Eye Institute) and Wayne State University School of Medicine MD/PhD program for DB. Received: JAccepted: NovemPublished: December 15, 2010Ĭopyright: © 2010 Holt et al. PLoS ONE 5(12):Įditor: Jun Yan, Hotchkiss Brain Institute, University of Calgary, Canada 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.Ĭitation: Holt AG, Bissig D, Mirza N, Rajah G, Berkowitz B (2010) Evidence of Key Tinnitus-Related Brain Regions Documented by a Unique Combination of Manganese-Enhanced MRI and Acoustic Startle Reflex Testing. Therefore, abnormal membrane depolarization in the DCIC appears to be important in tinnitus-mediated activity. ![]() Only in the dorsal cortex of the inferior colliculus (DCIC) did both models exhibit supernormal uptake. Neither model demonstrated significant differences in the auditory cortex. Salicylate-induced tinnitus resulted in wide spread supernormal manganese uptake compared to noise-induced tinnitus. 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. However, there are no diagnostic biomarkers for tinnitus-related pathophysiology for use in awake, freely moving animals. Animal models continue to improve our understanding of tinnitus pathogenesis and aid in development of new treatments. ![]()
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