Steven Green, PhD


Office: 238 BBE
Office Phone: 319-335-1612

Lab Website:

Neurotrophic signaling

We are interested in the molecular and cellular mechanisms by which afferent input affects neuronal physiology, synapses, and survival. We study the peripheral auditory system (cochlea). The neurons of the cochlea (spiral ganglion neurons, “SGNs”) have a single afferent input, the auditory sensory cells (hair cells). One question we ask is what is the consequence to neurons of loss of afferent input? Because hair cells can be selectively eliminated in vitro or in vivo, our system allows us to study the consequences of deafferentation to SGNs, and to so so, in parallel, in culture dishes or in the animal. Eliminating hair cells results in gradual degeneration or death of the SGNs. One application of our research is improvement of cochlear implants, the only effective treatment for deafness. These directly stimulate SGNs in the absence of hair cells but their function may be compromised by neuronal degeneration.

A second question is what is the consequence to SGNs of overactivity? Excessive excitation of SGNs by hair cells results in irreversible damage to the synapses between the hair cells and SGNs. We study this phenomenon in vitro with the aims of better understanding how cochlear synapses are damaged by excessive excitation (“excitotoxicity”), what can be done to protect cochlear synapses from excitotoxicity, and what intercellular signaling between hair cells and SGNs maintains synapses. Excitotoxic damage to cochlear synapses is one of the consequences of loud noise, is irreversible, and, while not necessarily causing immediate hearing loss, appears to exacerbate long-term hearing loss.

PubMed link

Department/Program Affiliations:
Molecular Medicine