Chronic cigarette smoke exposure drives spiral ganglion neuron loss in mice

Stephen T. Paquette, Ryan P. Dawes, Isaac K. Sundar, Irfan Rahman, Edward B. Brown & Patricia M. White - Department of Neuroscience, Ernest J. Del Monte Institute for Neuroscience, University of Rochester School of Medicine and Dentistry, USA

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.

How Amira-Avizo Software is used

Confocal stacks were imported into the Amira FEI software suite with the XImagePAQ extension. Deconvolution was performed using the iterative maximum likelihood estimation package. The stack was segmented and thresholded, and the Separate Objects function was used to reconstruct the individual SYP volumes. These were exported using the Connected Components function.