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Mechanisms of SGN-hair cell connectivity

The perception of sound occurs 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 moderate environmental noise leads to ribbon synapse loss and eventual SGN degeneration. Several projects in the lab focus on how factors such as semaphorins and purinergic receptors control distinct steps of SGN connectivity with hair cells.


 Photo above left: an early postnatal cochlea immunostained with anti-myosin 6 antibodies (blue; hair cells) and genetic labeling of sparse numbers of SGNs (from the Neurog1CreERT2 line from the Goodrich laboratory).  

Intercellular communication between SGNs and the cochlear mesenchyme

Pou3f4 is a transcription factor expressed by otic mesenchyme cells in the cochlea and mutations in Pou3f4 cause human hearing loss. Loss of Pou3f4 in mouse models leads to morphological defects in otic mesenchyme and these models are known to be hearing impaired as a result of reduced endocochlear potential. Several projects in the lab focus on the function of Pou3f4 in axon guidance, transcriptional regulation, and neuronal survival in the auditory system.


 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. 

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