Chronic cigarette smoke exposure drives spiral ganglion neuron loss in mice.
Stephen T PaquetteRyan P DawesIsaac K SundarIrfan RahmanEdward B BrownPatricia M WhitePublished in: Scientific reports (2018)
Tobacco use is associated with an increased risk of hearing loss in older individuals, suggesting cigarette smoke (CS) exposure may target the peripheral auditory organs. However, the effects of CS exposure on general cochlear anatomy have not previously been explored. Here we compare control and chronic CS exposed cochleae from adult mice to assess changes in structure and cell survival. Two-photon imaging techniques, including the imaging of second harmonic generation (SHG) and two-photon excitation fluorescence (TPEF) from native molecules, were used to probe the whole cochlear organ for changes. We found evidence for fibrillar collagen accumulation in the spiral ganglion and organ of Corti, consistent with fibrosis. Quantitative TPEF indicated that basal CS-exposed spiral ganglion neurons experienced greater oxidative stress than control neurons, which was confirmed by histological staining for lipid peroxidation products. Cell counts confirmed that the CS-exposed spiral ganglion also contained fewer basal neurons. Taken together, these data support the premise that CS exposure induces oxidative stress in cochlear cells. They also indicate that two-photon techniques may screen cochlear tissues for oxidative stress.
Keyphrases
- hearing loss
- oxidative stress
- induced apoptosis
- neuropathic pain
- spinal cord
- high resolution
- living cells
- optic nerve
- dna damage
- ischemia reperfusion injury
- diabetic rats
- high fat diet induced
- physical activity
- mass spectrometry
- endoplasmic reticulum stress
- high throughput
- young adults
- electronic health record
- cell therapy
- middle aged
- metabolic syndrome
- single cell
- cell death
- mesenchymal stem cells
- big data
- type diabetes
- cell cycle arrest
- energy transfer
- peripheral blood
- optical coherence tomography