Tejbeer Kaur, PhD

Tejbeer Kaur, PhD

Tejbeer Kaur, PhD

Assistant Professor
School of Medicine, Omaha Campus


  • Auditory Neuroscience
  • Hearing and Hearing Loss
  • Neuron Degeneration, Repair and Survival
  • Ototoxicity
  • Inflammation
  • Innate-Immune System
  • Mononuclear Phagocytes
  • Chemokines
  • Microglia
  • Sensory Hair Cell Damage and Loss

Academic Appointments


  • Biomedical Sciences


  • Assistant Professor


BS: Pharmacy, University of Delhi, India, 2005
MS: Pharmacology, University of Delhi, India,  2008
PhD: Pharmacology, Southern Illinois University, Carbondale, IL, 2012
Postdoctoral Research: Auditory Neurobiology, Washington University, St. Louis, MO, 2016


Publications and Presentations


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Research and Scholarship

Research and Scholarship Interests

  • To understand the biological mechanisms of neuron degeneration and their endogenous repair and survival in the mammalian auditory system with a long-term goal to develop therapies to preserve or restore hearing.

Current Research Projects

  • The mammalian hearing organ, the cochlea, contains sensory epithelium, the organ of Corti that consists of hair cells (sensory receptors) responsible for converting sound into electrical signals that are conveyed to the brain via bipolar afferent spiral ganglion neurons (SGNs). The loss of hair cells or their connections with SGNs (termed “ribbon synapses”) results in sensory neural hearing loss (SNHL). Hair cell or synaptic loss is often followed by gradual degeneration and ultimately death of SGNs. Such pathology occurs after noise overexposure, treatment with certain medications, infection or ageing and is heterogenous in nature. SNHL is often permanent, leading to lifelong challenges in speech recognition and listening in noisy environments. The primary therapies for SNHL are amplification devices, such as hearing aids, and cochlear implants. But the effectiveness of these devices is extremely limited in people whose SNHL is due to deficient or absent auditory nerve innervation and cell bodies. SGNs do not regenerate spontaneously and there are currenlty no FDA approved drugs that promote neuron survival or elicit neuron regeneration or synaptogenesis. The mechanisms of SGN degeneration and loss are poorly understood. Thus, our overarching goal is to determine the biological mechanisms of SGN degeneration, repair and survival to develop better therapies for neuroprotection and regeneration to preserve or restore hearing.
         Inflammation is a hallmark of SNHL. Macrophages (innate-immune cells), the primary responders of inflammation are increased and activated as a result of damage to the cochlea. However, the precise function of inflammation and macrophages in cochlear pathology and hearing loss remains unclear. Our research work has shed light on novel and beneficial roles of macrophages in promoting the long-term survival of auditory neurons and repair of damaged synapses in the injured cochlea (Kaur et al., J Neuroscience, 2015; Kaur et al., J Comparative Neurology, 2018; Kaur et al., Frontiers in Neuroscience, 2019). This research work has also led to the identification of a neuron-immune molecular signaling, fractalkine signaling, that can regulate neuron survival and synaptic repair in damaged cochlea. Fractalkine signaling is a unique neuron-immune-ligand-receptor pair where chemokine fractalkine (CX3CL1) is constitutively expressed on SGNs and binds to its exclusive receptor CX3CR1 expressed by macrophages. Our findings have revealed a critical role for immune system in auditory pathology and suggest that macrophages and fractalkine play a neuroprotective role in the damaged cochlea. A more complete understanding of how macrophages and fractalkine regulate neuron survival and synaptic repair will provide critical information towards developing novel immunotherapies to prevent auditory nerve degeneration or promote nerve regeneration and re-establishment of their synaptic connections and restore hearing.

    Research Techniques
    Mouse genetics, RNA sequencing, confocal imaging of fixed and live tissue, super-resolution imaging, cellular and molecular biology techniques, fluorescent immunohistochemistry, cochlear explant culture, cochlear microdissections, histology, auditory function assessment, flow cytometry, cell sorting, immunophenotyping.
    Learn more about our research here:

Grant Funding Received

  • R03 DC015320 NIH/NIDCD Period: 04/2016 – 07/2019 Role: PI $450,000 (total) Role of macrophages in noise-induced cochlear synaptopathy and neuropathy.

Awards and Honors

  • Co-Chair, Association for Research in Otolaryngology, 2021
  • Guest Associate Editor, Frontiers in Neuroscience and Cellular Neurophysiology , 2020
  • Panelist, Job Search and Independence, spARO Mentoring Session, 43rd Association for Research in Otolaryngology MidWinter Meeting, 2020