Manoj Kumar, Ph.D.
Meet the Researcher
Kumar received his doctorate in neuroscience and pharmacology from West Virginia University and completed his postdoctoral research in the department of otolaryngology at the University of Pittsburgh, where he is currently a research assistant professor. His 2025 Emerging Research Grant is generously funded by Hyperacusis Research.
Kumar is also a 2022–2023 ERG scientist, generously funded by Royal Arch Research Assistance. Click here to read his Meet the Researcher profile from 2022.
The Research
University of Pittsburgh
KCNQ2/3 potassium channel activator mitigates noise-trauma–induced hypersensitivity to sounds in mice
Noise-induced hearing loss (NIHL) is one of the most common causes of hearing disorders. NIHL reduces the auditory sensory information relayed from the cochlea to the brain, including the primary auditory cortex (A1). To compensate for reduced peripheral sensory input, A1 undergoes homeostatic plasticity. Namely, the sound-evoked activity of A1 excitatory principal neurons (PNs) recovers or even surpasses pre-noise trauma levels and exhibits increased response gain (the slope of neuronal responses against sound levels). This increased gain of A1 PNs after NIHL is associated with highly debilitating hearing disorders, such as tinnitus (perception of phantom sounds), hyperacusis (painful perception of sounds), and hypersensitivity to sounds (increased sensitivity to everyday sounds). Despite the high prevalence of these hearing disorders, treatment options are limited to cognitive behavioral therapy and hearing prosthetics with no FDA-approved pharmacotherapeutic options available. Therefore, to aid in the development of pharmacotherapeutic options, it is imperative to 1) develop animal models of these hearing disorders, 2) identify the brain plasticity underlying these hearing disorders, and 3) test potential pharmacotherapy to rehabilitate hearing and brain plasticity after NIHL. Here, we aim to develop a novel mouse model of hypersensitivity to sounds, identify its underlying A1 plasticity, and test pharmacotherapy to mitigate it after NIHL.
Long-term goal: The long-term goals of this project are to identify the molecular, cellular, and circuit mechanisms underlying the plasticity of the auditory cortex after noise-induced hearing loss (NIHL). Based on our findings, future studies will investigate the causal role of several neuron types in the development of hypersensitivity to sounds and hyperacusis after NIHL and the synaptic and intrinsic mechanisms underlying the plasticity of these neurons after NIHL. Determining the inhibitory circuit mechanisms underlying the plasticity of the auditory cortex (AC) after NIHL will reveal novel therapeutic targets for treating and rehabilitating the impaired hearing after NIHL. Also, because AC plasticity is associated with hyperexcitability-related disorders such as tinnitus and hyperacusis, a detailed mechanistic understanding of AC plasticity will highlight the path for the development of novel treatments for these disorders. Moreover, our findings will provide insights into AC plasticity occurring in hearing loss induced by ototoxic drugs or ear diseases and in other pathologically increased central gain disorders, like tinnitus and hyperacusis.
