Poster abstracts

Poster number 81 submitted by Ben Seicol

Cochlear inflammation in CBA/CaJ mice increases during age-related hearing loss

Benjamin J Seicol (Department of Otolaryngology, Department of Neuroscience), Ruili Xie (Department of Otolaryngology, Department of Neuroscience)

Abstract:
Age-related hearing loss (ARHL) is major hearing impairment in patients that is widely studied in research animals. Hair cells in the cochlea transduce mechanical sound waves into electrical signals, and specialized ribbon synapses reliably transmit precise auditory information to the peripheral terminals (cochlear synapses) of spiral ganglion neurons. Loss of hair cells and cochlear synapses lead to sensorineural hearing loss in ARHL. CBA/CaJ mice exhibit late-onset, human-like progression of hearing loss during normal aging making them a fitting model for studying ARHL in mice. Cochlear macrophages and circulating monocytes drive cochlear inflammation following physical and chemical insults to cochlea, and in humans, cochlear inflammation has recently been confirmed in post-mortem tissue samples of aged patients. However, well-controlled animal studies of cochlear inflammation in late-onset ARHL are needed to advance our mechanistic understanding of the contribution of inflammation to sensorineural hearing loss in aging. To address this, we have conducted a series of immunohistochemical studies examining cochlear inflammation in aged (~30 months) and young (~2-3 months) CBA/CaJ mice. Iba1-labeled resident macrophages show increased area and elevated levels of CD68, indicating increased activation, corresponding with age. This descriptive study confirms that CBA/CaJ mice are a suitable model system for studying inflammation in ARHL and indicates that ARHL-associated inflammation may contribute to the pathophysiology of hearing loss.

Keywords: Cochlea, Aging, Inflammation