Journal
EXPERIMENTAL AND MOLECULAR PATHOLOGY
Volume 119, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yexmp.2021.104605
Keywords
GABA; glutamate homeostasis; Blast exposure; Blast overpressure; Chinchilla; Tinnitus; Mass spectrometry imaging
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Funding
- National Institutes of Health through the National Center for Research Resources [S10RR029517-01]
- Hearing Health Foundation
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Acoustic trauma can damage inner ear neural structures, leading to hearing loss and neurotransmitter imbalances that may cause tinnitus. Studies using chinchilla models have provided new insights into the pathomechanism of tinnitus.
Acoustic trauma damages inner ear neural structures including cochlear hair cells which result in hearing loss and neurotransmitter imbalances within the synapses of the central auditory pathway. Disruption of GABA/ glutamate levels underlies, tinnitus, a phantom perception of sound that persists post-exposure to blast noise which may manifest in tandem with acute/chronic loss of hearing. Many putative theories explain tinnitus physiology based on indirect and direct assays in animal models and humans, although there is no comprehensive evidence to explain the phenomenon. Here, GABA/glutamate levels were imaged and quantified in a blast overpressure model of chinchillas using Fourier transform ion cyclotron resonance mass spectrometry imaging. The direct measurement from whole-brain sections identified the relative levels of GABA/glutamate in the central auditory neuraxis centers including the cochlear nucleus, inferior colliculus, and auditory cortex. These preliminary results provide insight on the homeostasis of GABA/glutamate within whole-brain sections of chinchilla for investigation of the pathomechanism of blast-induced tinnitus.
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