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We study how nerves from the brain communicate with sensory hair cells in the inner ear. We are particularly interested in how this communication changes with age, what drives these changes and whether manipulating this communication can protect our ears from age-related hearing loss.

Do you find yourself asking people to speak louder or repeat what they have said? Or do you have an older relative that struggles to hear what you’re saying? Age-related hearing loss (ARHL), also known as presbycusis, is the most common health condition in the elderly. This progressive loss of hearing can have a huge effect on someone’s ability to communicate, especially in social situations, leaving people feeling isolated and even depressed. Given the ageing population, this condition is something that needs to be addressed. Currently, we have a poor understanding of the cellular changes that occur within the cochlea throughout the process of ageing and so our research aims to rectify this.

Using techniques such as electrophysiology, immunohistochemistry and two-photon imaging, we aim to understand how the communication between three cell types within the cochlea changes with age. These cell types are the sensory hair cells (also known as inner hair cells), the sensory neurons (also known as afferent neurons) and the motor neurons (also known as efferent neurons). The inner hair cells convert the mechanical energy of sound into electrical impulses which can be communicated with the afferent neurons. The afferent neurons in turn carry this information about sound to the brain. The information that the afferent neurons carries to the brain can be modulated by the efferent neurons; these are neurons that originate in the brain and project to the cochlea.

We know that the number of connections between the inner hair cells and the afferent neurons is reduced during ageing. There is also evidence suggesting that the efferent neurons stop communicating with the afferent neurons with age and instead start communicating directly the inner hair cells. We are interested in understanding these changes further by determining which changes occur first and what the molecular mechanisms are that underpin them.

We believe that in understanding these changes better we can identify novel targets and pharmacological interventions that could enable us to manipulate these cells so that they maintain the same communication pattern as that found in a healthy cochlea, and therefore reduce ARHL.