Exploring mechanisms of hearing, deafness and auditory disease

The Auditory Nerve: Blair Grubb & Mike Mulheran

Sound is detected by hair cells in the cochlea and encoded as precisely timed action potential trains in the spiral ganglion neurons (SGN) which project into the brain (along the 8th nerve). High levels of sound that damage the inner ear also cause profound changes in SGN excitability which contributes to deafness and tinnitus.

Plasticity in the Cochlear Nucleus: Martine Hamann

The SGN project into two divisions of the cochlear nucleus. The dorsal division (DCN) is considered analogous to the circuitry of the cerebellum, and integrates auditory and other somato-sensory information. Acute acoustic over-exposure modulates synaptic inputs and firing properties of fusiform cells within this region.

Auditory Processing in the Brainstem: Conny Kopp-Scheinpflug & Ian Forsythe

The ventral division of the cochlear nucleus provides several projections into the superior olivary complex (SOC) where the medial and lateral superior olives (LSO & MSO) compare information from both ears for localization of sound in auditory space. The superior paraolivary nucleus (SPN) performs sound gap-detection, essential for speech comprehension.

How the Aging Brain can exacerbate Deafness: Margaret Barnes-Davies & Ian Forsythe

The ventral nucleus of the trapezoid body (VNTB)  controls sound amplification in the cochlea via the olivocochlear bundle (OCB). A project funded by Action for Hearing Loss and Age-UK is investigating the hypothesis that age-related hearing loss may in part be explained by failures in this system.

The calyx of Held & the Control of Neuronal Excitability: Ian Forsythe

This giant excitatory synapses provides an important model synapse for investigation of synaptic transmission, funded by the Medical Research Council (MRC) and Wellcome Trust. We have shown how synaptic activity at the calyx induces volume transmission through nitric oxide signalling to control the intrinsic excitability of surrounding neurons. This phenomenon contributes to auditory processing and auditory disease associated with hyperbilirubinaemia. This work is funded by Deafness Research UK and Action on Hearing Loss . 

Mechanisms of Auditory Injury and Disease

Loud sound causes deafness by damage to the hair cells in the cochlea but can also compromise hearing by changing the way the brain processes sound, thereby altering sound perception. These central changes exacerbate or perhaps mitigate, the peripheral injury in deafness and may underlie phenomena such as tinnitus.

Martine Hamann has received funding from Action on Hearing Loss and the Leicester Neuroscience Theme to set up methods to explore tinnitus induction, as part of a wider collaboration across the Leicester group and with the MRC Institute for Hearing Research in Nottingham. A further project is funded by East Midlands Development Association (EMDA) and the UK Design Council for Mike Mulheran in assisting the development of a novel light therapy for tinnitus. Knowledge of potassium ion channels in controlling neuronal excitability is being exploited by Ian Forsythe in collaboration with a GSK spin-out company, Autifony Therapeutics, for the development of agents to treat noise-induced hearing loss.  Action on Hearing Loss are funding studies of brain damage following severe hyperbilirubinaemia (Jaundice). Continuing links with the ENT department (Messrs Peter Rea, Anil Banerjee & Henry Pau) at the Leicester Royal Infirmary have contributed to successful clinical trials for tinnitus therapeutics (Merz, Neramexane) and light therapy research (Orthoscopics) and in developing strategies for neuroprotection in the ear and brain.

Please contact: Professor Ian Forsythe, or the specific individuals above, if you wish to discuss research opportunities.