Timothy Balmer, Ph.D.

Meet the Researcher

Balmer earned his doctorate in neuroscience from Georgia State University. He is an assistant professor in the School of Life Sciences at Arizona State University. His work investigates how neurons transmit signals to one another through synapses and how networks of neurons process information. His team uses in vitro and in vivo electrophysiology, optogenetics, immunohistochemistry, and computational modeling, to understand fundamental mechanisms of sensory processing. Balmer is a 2025 Emerging Research Grants recipient generously funded by the Salice Family Foundation.

Balmer is also a 2022–2023 ERG scientist for an earlier Ménière’s disease project, generously funded by an anonymous donor, and a 2017 ERG scientist for a tinnitus project that was generously funded by the Les Paul Foundation. Click here to download a PDF of Dr. Balmer's Meet the Researcher profile from 2017, when his tinnitus research was funded.

The Research

Arizona State University

The role of NMDA receptors in vestibular circuit function and balance

The vestibular cerebellum is the part of the brain that integrates signals that convey head, body and eye movements to coordinate balance. When this neural processing is disrupted by central or peripheral vestibular disorders, profound instability, vertigo, and balance errors result. We lack a basic understanding of the development and physiology of the first vestibular processing region in the cerebellum, the granule cell layer. This lack of knowledge is a major roadblock to the development of therapies that could ameliorate peripheral disorders such as Ménière’s disease.

This project will look at a specific understudied cell type in the granule cell layer of the cerebellum, unipolar brush cells (UBCs). Our focus is particularly on the cells’ glutamate receptors, which control synaptic communication. It remains unclear how glutamate receptors assume their form and function during development, and we hypothesize that the NMDA-type glutamate receptors expressed by developing UBCs are necessary for the development of the remarkable dendritic brush of these cells, which slows and controls communication across the synapse, and the cells’ function in the circuit.

Long-term goal: The long-term goal of the proposed research is to understands how cerebellum-like circuits function and how their disruption may lead to hearing loss, tinnitus, and vestibular disorders. This requires understanding how the different cell types in cerebellum-like circuits develop, how they process signals, and how they influence the activities of one another. The least well understood cell-type in cerebellum-like circuits may be the unipolar brush cell (UBC). UBCs are excitatory interneurons that are present in the cochlear nucleus and vestibular cerebellum. They receive multisensory input and project axons to hundreds of other excitatory neurons, amplifying feedforward excitation. Identifying how UBC activity can be modified pharmacologically and how these manipulations impact circuit excitability is a major long-term goal. For example, reducing DCN output by reducing UBC excitability with drugs could reduce tinnitus. There are a variety of receptors and ion channels that UBCs express rather specifically that could be targeted to fine-tune UBC activity to potentially provide relief to tinnitus sufferers and suffers of vestibular sensory disorders, such as Ménière’s, as well.