RESEARCH INTERESTS
Mechanisms of SGN-hair cell connectivity
Hearing begins when sound waves enter the ear and are converted into neural impulses by specialized cells in the cochlea. Two cell types we focus on in our research are hair cells and spiral ganglion neurons (SGNs). To communicate auditory input to the brain, hair cells release glutamate onto SGNs at structures termed ribbon synapses. Previous work has shown that SGNs must be maintained for both normal hearing and for the function of cochlear implants and hearing aids. Recently, it was revealed that environmental noise leads to ribbon synapse loss and eventual SGN degeneration. In our research program, we are defining the mechanisms that control aspects of SGN-hair cell connectivity, including axon guidance, synapse formation, neuron survival, and prehearing spontaneous activity.
Intercellular communication between SGNs and the cochlear mesenchyme
POU3F4 is a transcription factor expressed by otic and vestibular mesenchyme cells. Mutations in Pou3f4 are associated with DFNX2, X-linked deafness with balance disorders. Several projects in the lab focus on the function of POU3F4 in axon guidance, transcriptional regulation, neuronal survival, and spontaneous activity in the inner ear.
Left: a whole-mount preparation of a cochlea immunostained with anti-Tuj1 (green; SGNs and efferents), anti-Sox10 (blue; glia) and anti-Pou3f4 (red; mesenchyme) antibodies.
