Molecular composition and function of the spiral ganglion neuron peripheral synapse in mice
The spiral ganglion neuron peripheral dendrite is the most vulnerable part of the auditory system and is thought to be lost following strong activation of the auditory system. Currently it is unclear which molecular processes lead to loss of these neuronal dendrites. In this thesis I examine both the molecular architecture and the molecular processes in the SGN peripheral dendrites to investigate which molecular processes could lead to spiral ganglion neuron damage. I first identify potassium ion channels as likely contributors to molecular processes that lead to neuronal dendrite loss. Subsequently, I identify the novel potassium ion channel KNa1 in the spiral ganglion neurons and determine that loss of these ion channels alters the activity patterns of the spiral ganglion neurons. Follow-up research indicates that loss of these ion channels increases auditory pathology with noise exposure and with increasing age. These findings identify the KNa1 channels in the spiral ganglion neurons and indicate that they have an important function in controlling the activity of spiral ganglion neurons and this likely protects the spiral ganglion neurons. These findings are important because they prove that potassium channels, and the KNa1 channel in particular, have a protective molecular function. Further elucidation of how potassium channels contribute to the overall activity and vulnerability of the spiral ganglion neurons would, therefore, contribute to our understanding of how the spiral ganglion neurons are damaged following activation of the auditory system.